Thijssen et al. reported factors affecting the diameters of the thoracic aorta in participants (1). By using non-enhanced cardiac CT, the diameters of the ascending (AA) and descending aorta (DA) were measured. The median absolute change in diameters during follow-up with mean scan interval of 14.1 years, was 1 mm for both the AA and DA. Absolute changes per decade in AA and AD diameters were significantly larger in males than in females. Significant determinants of changes in AA diameter were age, body mass index (BMI) and diastolic blood pressure (DBP) in female, and BMI in males. In addition, significant determinants of changes in DA diameter were age, BMI, DBP, and current smoking in female, and age and BMI in males. I have a comment about the study.
There are some sex differences in significant determinants for the change of AA and AD diameters, and BMI is a common risk factor. Ferrara et al. reported that there were no effects of gender, BMI, AA diameter, aortic stiffness index, smoking habits, diabetes mellitus, and Marfan syndrome on AA tissue in patients with AA aneurysms. In contrast, aging and hypertension made the AA tissue weaker (2). The significant determinants for dilation of AA and DA diameters may not directly relate to the risk of thoracic aneurysm, and BMI management is important to prevent thoracic aorta dilations in general population.
Reference
1. Thijssen CGE, Mutluer FO, van der Toorn JE, et al. Longitudinal changes of thoracic...
Thijssen et al. reported factors affecting the diameters of the thoracic aorta in participants (1). By using non-enhanced cardiac CT, the diameters of the ascending (AA) and descending aorta (DA) were measured. The median absolute change in diameters during follow-up with mean scan interval of 14.1 years, was 1 mm for both the AA and DA. Absolute changes per decade in AA and AD diameters were significantly larger in males than in females. Significant determinants of changes in AA diameter were age, body mass index (BMI) and diastolic blood pressure (DBP) in female, and BMI in males. In addition, significant determinants of changes in DA diameter were age, BMI, DBP, and current smoking in female, and age and BMI in males. I have a comment about the study.
There are some sex differences in significant determinants for the change of AA and AD diameters, and BMI is a common risk factor. Ferrara et al. reported that there were no effects of gender, BMI, AA diameter, aortic stiffness index, smoking habits, diabetes mellitus, and Marfan syndrome on AA tissue in patients with AA aneurysms. In contrast, aging and hypertension made the AA tissue weaker (2). The significant determinants for dilation of AA and DA diameters may not directly relate to the risk of thoracic aneurysm, and BMI management is important to prevent thoracic aorta dilations in general population.
Reference
1. Thijssen CGE, Mutluer FO, van der Toorn JE, et al. Longitudinal changes of thoracic aortic diameters in the general population aged 55 years or older. Heart 2022 doi: 10.1136/heartjnl-2021-320574
2. Ferrara A, Totaro P, Morganti S, et al. Effects of clinico-pathological risk factors on in-vitro mechanical properties of human dilated ascending aorta. J Mech Behav Biomed Mater 2018;77:1-11.
In the investigation recently published in “Heart”, the authors discuss the efficacy of beta blockade in treating individuals with the Takotsubo cardiomyopathy. [1] Another recent publication shows this to be a controversial topic. [2] These discussions emphasize the significance of the dose-related sensitivity of one component of three-dimensional aggregation of the ventricular cardiomyocytes, a feature which, thus far, has received little attention. Intraoperative cardio-dynamic measurements [3] have shown that the cardiomyocytes within the three-dimensional mesh that are aggregated in intruding, as opposed to tangential, fashion are statistically more sensitive to both positive and negative inotropes when given at low doses. The cardiomyocytes aggregated in transmural fashion exert a dilatory effect, in contrast to the tangential aggregates, which act exclusively to drive ventricular ejection. The different functions of the two populations indicates that the ventricular cone, as a whole, functions as an antagonistic system. [4]
When the ventricular walls are hypertrophied in response to increased resistance to flow, ventricular wall thickening stretches and tilts the cardiomyocytes aggregated in transmural fashion, thus increasing the dilating forces. At the same time, of course, the transmural cardiomyocytes themselves undergo hypertrophy. This triggers a vicious circle, with both populations of cardiomyocytes undergoing hypertrophy. In this situation, however,...
In the investigation recently published in “Heart”, the authors discuss the efficacy of beta blockade in treating individuals with the Takotsubo cardiomyopathy. [1] Another recent publication shows this to be a controversial topic. [2] These discussions emphasize the significance of the dose-related sensitivity of one component of three-dimensional aggregation of the ventricular cardiomyocytes, a feature which, thus far, has received little attention. Intraoperative cardio-dynamic measurements [3] have shown that the cardiomyocytes within the three-dimensional mesh that are aggregated in intruding, as opposed to tangential, fashion are statistically more sensitive to both positive and negative inotropes when given at low doses. The cardiomyocytes aggregated in transmural fashion exert a dilatory effect, in contrast to the tangential aggregates, which act exclusively to drive ventricular ejection. The different functions of the two populations indicates that the ventricular cone, as a whole, functions as an antagonistic system. [4]
When the ventricular walls are hypertrophied in response to increased resistance to flow, ventricular wall thickening stretches and tilts the cardiomyocytes aggregated in transmural fashion, thus increasing the dilating forces. At the same time, of course, the transmural cardiomyocytes themselves undergo hypertrophy. This triggers a vicious circle, with both populations of cardiomyocytes undergoing hypertrophy. In this situation, however, as emphasized, the dilatory activity can selectively be damped by low dosage beta – blockade. [5] This potential has been shown in a baby born with right ventricular hypertrophy, when the beta-blockers given at low doses produced complete remission of the hypertrophy [6].
Biopsies have confirmed that myocardial hypertrophy is part and parcel of the of Takotsubo cardiomyopathy [7]. It is likely that, in this setting, selective hypertrophy of the transmural aggregates is induced by the slightly elevated levels of adrenalin known to prevail in these patients [8]. Selective damping of the transmural aggregates by low dose beta-blockade, therefore, can be anticipated to be a more appropriate treatment than use of the higher doses, as currently recommended. [1,2]
References:
1: Silverio A, Parodi G, Scudiero F, Bossone E , Di Maio M Vriz O et al [2022] Beta-blockers are associated with better long-term survival in patients with Takotsubo syndrome . Heart 108(17):1369-1376. doi: 10.1136/heartjnl-2021-320543.
2: Kummer M, El-Battrawy I, Gietzen T, Ansari U, Behnes M, Lang S, Zhou X Borggrefe M , Akin I [ 2020] The Use of Beta Blockers in Takotsubo Syndrome as Compared to Acute Coronary Syndrome. Front Pharmacol. 211: 681-689 doi: 10.3389/fphar.2020.00681
3: Lunkenheimer PP, Redmann K, Cryer CW, Batista RIV, Stanton JJ, Niederer P, Anderson RH (2007) Beta-blockade at low doses restoring the physiological balance in myocytic antagonism. Eur J Cardio Thorac Surg 32: 225-230, DOI: 10.1016/j.ejcts.2007.03.048
4: Lunkenheimer PP, Redmann K, Hoffmeier A, Niederer P, Stephenson R, Schmitt B, L Theilmann L, Becker F, Anderson RH (2017) The Ventricular Structure Functioning as an Antagonistic Continuum. J Biomed Tech Res 3 (1): 104-114
5: Schmitt B, Li T, Kutty SH, Klasheei AL, Schmitt KRL, Anderson RH, Lunkenheimer PP, Berger F, Kühne T, Peters B (2015) Effects of incremental beta-blocker dosing on myocardial mechanics of the human left ventricle: MRI 3D-tagging insight into pharmacodynamics supports theory of inner antagonism. Am J Physiol Heart Circ Physiol 309:H45-52, DOI: 10.1152/ajpheart.00746.2014
6: Emeis M, Lunze FI, Miera O, Berger F, Rossi R, Schmitt B. (2020) Congenital hypertrophy of the right ventricle successfully treated with very low dose beta blockers. Cardiology and Cardiovascular Medicine 4,760-765
7: Nef HM, Möllmann H, Kostin S, Troidl C, Voss S, Weber M, Dill T, Brandt R, Hamm CW [2007] Takotsubo cardiomyopathy: intraindividual structural analysis in the acute phase and after functional recovery. European Heart Journal 28, 20: 2456–2464, https://doi.org/10.1093/eurheartj/ehl570
8: Templin C, Hänggi J, Klein , et al. [2019] Altered limbic and autonomic processing supports brain-heart axis in takotsubo syndrome. European Heart Journal. 40(15):1183–1187. doi: 10.1093/eurheartj/ehz068.
I take great concern in regards to the conclusions that this and multiple other previous cardiology articles have laid claim to in regards to calcium supplementation. Many providers read these articles and tell patients to stop taking calcium, this then results in osteoporosis and fractures which also has a high mortality rate. There must be significant caution in making the conclusions that this article makes. The amount of calcium the patients were taking was quite varied between 500-2,000 mg a day, patients with bone disease need 1200 mg a day in order to maintain normal bone turnover and rebuilding by the osteoblast. There needs to be data from this study showing the poor outcome patient’s calcium supplement amounts. To insinuate that all calcium supplements are bad is not only a disservice but a detriment to our patients. Patients now have access to articles more than ever and will read this and now won’t take their calcium supplements, this means that anyone treating osteoporosis will now have to explain this and other articles. Patients are more likely to believe bad data than good data. The truth is that calcium is needed for good bone health and there is a safe amount that is not a risk to cardiac health. This article amongst others does not bring in that side of the story.
To the Editor
We read with interest the recent review by Griborio-Guzman AG et al [1] of the clinical presentation, diagnosis and management of cardiac myxomas. The authors highlighted that cardiac myxomas should be managed with prompt resection. Yet, the question of whether excision of an atrial myxoma qualifies as an emergency procedure remains unanswered.
In an attempt to address this question, we constructed a “best evidence topic” according to a structured protocol, as described previously [2]. A comprehensive MEDLINE literature search was conducted utilizing the PubMed interface (1966-August 2021) using the keywords: [(atrial myxoma) OR (cardiac myxoma) OR (heart myxoma)] AND [(resection) OR (removal) OR (excision)] AND [(emergency) OR (urgent) OR (immediate) OR (prompt)]. References of selected articles were then reviewed to detect relevant publications that did not come up with the original search. Two hundred and fifty-six papers were found using the reported search. From these, 11 papers were identified that provided best evidence to answer the question, all of them were single-group case-series.
In one of the earliest clinical series, Semb et al [3] emphasized that surgery should be performed as soon as the diagnosis is made, and observed that tumour fragmentation and embolization was more likely to occur when a lobulated, gelatinous and fragile myxoma was located in the central bloodstream.
Livi et al [4] reported that sudden death could...
To the Editor
We read with interest the recent review by Griborio-Guzman AG et al [1] of the clinical presentation, diagnosis and management of cardiac myxomas. The authors highlighted that cardiac myxomas should be managed with prompt resection. Yet, the question of whether excision of an atrial myxoma qualifies as an emergency procedure remains unanswered.
In an attempt to address this question, we constructed a “best evidence topic” according to a structured protocol, as described previously [2]. A comprehensive MEDLINE literature search was conducted utilizing the PubMed interface (1966-August 2021) using the keywords: [(atrial myxoma) OR (cardiac myxoma) OR (heart myxoma)] AND [(resection) OR (removal) OR (excision)] AND [(emergency) OR (urgent) OR (immediate) OR (prompt)]. References of selected articles were then reviewed to detect relevant publications that did not come up with the original search. Two hundred and fifty-six papers were found using the reported search. From these, 11 papers were identified that provided best evidence to answer the question, all of them were single-group case-series.
In one of the earliest clinical series, Semb et al [3] emphasized that surgery should be performed as soon as the diagnosis is made, and observed that tumour fragmentation and embolization was more likely to occur when a lobulated, gelatinous and fragile myxoma was located in the central bloodstream.
Livi et al [4] reported that sudden death could occur due to complete obstruction of valvular orifice, and this convinced the authors of the necessity of a prompt operation once the diagnosis is made, regardless of the size and location of the tumour.
Sugimoto et al [5] believed that a cardiac myxoma should be excised as soon as possible because it may produce serious complications. While optimal timing of surgery after the onset of embolic complications (especially cerebral or myocardial infarction) remained controversial, the authors believed that early surgery may have to be performed when there is a threat of new embolic events.
Lijoi et al [6] advocated that surgical excision is undertaken as soon as possible after diagnosis in order to avoid such complications as systemic embolization and valvular incompetence with rapid deterioration.
Meyns et al [7] noted that embolization was not related to the size of the myxoma, but was dictated by the friability of the tissues. The authors recommended immediate excision of atrial myxoma once the diagnosis is established.
Keeling et al [8] highlighted that embolization risk was increased in patients presenting with a cardiac rhythm other than sinus rhythm, and in large, left-sided, polypoid and mitral valve myxomas. Their study concluded that immediate resection of cardiac myxomas should be performed to prevent sudden death and embolic events and that, by immediate resection, these risks may be very low.
Selkane et al [9] advocated that surgery for cardiac myxoma should comply with the usual recommendations for preoperative coronary angiography, and that emergency surgery should be available to acute symptomatic patients and those at a high risk of embolization.
Khan et al [10] performed immediate surgical treatment in all their patients, and this was associated with low rates of morbidity and mortality. The authors recommended that surgical excision should be carried out without delay, while coronary angiography was advised if coronary artery disease is suspected or if patient’s age was over 40 years.
Kuroczyński et al [11] recommended urgent resection of cardiac myxomas after establishing the diagnosis to prevent complications such as embolization or obstruction of the mitral orifice. They also recommended performing pre-operative coronary angiography in patients aged over 40 with risk factors for coronary heart disease.
Garatti et al [12] recommended that surgical excision of cardiac myxomas must be done as soon as possible after the diagnosis is established because of the high risk of valvular obstruction or systemic embolization.
Lastly, Rushel et al [13] believed that immediate surgical excision was indicated in all patients to prevent sudden death and embolic complications.
In summary, our “best evidence topic” review indicates that, even though comparative data is lacking, there is sufficient data to indicate that excision of an atrial myxoma qualifies as an emergency procedure in acute symptomatic patients, where acute valvular obstruction was conceivable (such as in large mobile left atrial myxomas) and where tumour embolization was more likely to occur (e.g. lobulated and gelatinous myxomas). Excision of other atrial myxomas can be performed on an urgent basis, which allows for a thorough preoperative optimization and assessment (including coronary angiography).
References
1. Griborio-Guzman AG, Aseyev OI, Shah H, Sadreddini M. Cardiac myxomas: clinical presentation, diagnosis and management. Heart. 2021 Sep 7:heartjnl-2021-319479. doi: 10.1136/heartjnl-2021-319479
2. Dunning J, Prendergast B, Mackway-Jones K. Towards evidence-based medicine in cardiothoracic surgery: best BETS. Interact CardioVasc Thorac Surg 2003, 2:405-9
3. Semb BKH. Surgical considerations in the treatment of cardiac myxoma. J Thorac Cardiovasc Surg 10984; 87:251-259
4. Livi U, Bortolotti U, Milano A, Valente M, Prandi A, Frugoni C, de Mozzi P, Valfre C, Mazzucco A, Gallucci V. Cardiac myxomas: results of 14 years' experience. Thorac Cardiovasc Surg. 1984; 32:143-7
5. Sugimoto T, Ogawa K, Asada T, Mukohara N, Nishiwaki M, Higami T, Kawamura T. Surgical treatment of cardiac myxoma and its complications. Cardiovasc Surg. 1993; 1:395-8
6. Lijoi A, Scoti P, Faveto C, Canale C, Parodi E, Passerone GC, Dottori V, Venere G. Surgical management of intracardiac myxomas. A 16-year experience. Tex Heart Inst J. 1993; 20:231-4
7. Meyns B, Vancleemput J, Flameng W, Daenen W. Surgery for cardiac myxoma. A 20-year experience with long-term follow-up. Eur J Cardiothorac Surg. 1993; 7:437-40
8. Keeling IM, Oberwalder P, Anelli-Monti M, Schuchlenz H, Demel U, Tilz GP, Rehak P, Rigler B. Cardiac myxomas: 24 years of experience in 49 patients. Eur J Cardiothorac Surg. 2002; 22:971-7
9. Selkane C, Amahzoune B, Chavanis N, Raisky O, Robin J, Ninet J, Obadia JF. Changing management of cardiac myxoma based on a series of 40 cases with long-term follow-up. Ann Thorac Surg. 2003; 76:1935-8
10. Khan MA, Khan AA, Waseem M. Surgical experience with cardiac myxomas. J Ayub Med Coll Abbottabad. 2008; 20:76-9
11. Kuroczyński W, Peivandi AA, Ewald P, Pruefer D, Heinemann M, Vahl CF. Cardiac myxomas: short- and long-term follow-up. Cardiol J. 2009; 16:447-54
12. Garatti A, Nano G, Canziani A, Gagliardotto P, Mossuto E, Frigiola A, Menicanti L. Surgical excision of cardiac myxomas: twenty years’ experience at a single institution. Ann Thorac Surg. 2012; 93:825-31
13. Rushel SS, Mandal SC, Moinuddin S, Alamgir MK. Surgical Treatment of Cardiac Tumours: a 17-year Experience at Department of Cardiac Surgery, NICVD, Dhaka. Mymensingh Med J. 2019; 28:562-566
In an initial review and meta-analysis, Rizos et al1 stated that omega-3 supplementation at low and higher dosages showed no or weak associations with cardiovascular disease (CVD) outcomes. Then, we reported more recent reviews that displayed a protective activity of omega-3 supplementation against CVD outcomes.2 Moreover, we reported that both metabolic syndrome (MetS) and Helicobacter pylori infection (Hp-I) increase the risk of cardio-cerebrovascular events, the endpoint of MetS,2 and omega-3 acids are beneficial against these disorders.2 Next, a corresponding piece commenting on our own paper by Rizos et al,3 reported that some recent data showed, for instance, low and/or high dosage of omega-3 supplementation was not associated with CVD outcomes.3 However, multiple trials continue to use low dosage of omega-3, which demonstrated substantial CVD benefits and other recent data showed that higher dosage of omega-3 (4 g/day) also induced a remarkable reduction in CVD events.4 The current contradictory findings can be attributed to several contributors including diverse types of omega-3 fatty acids (only eicosapentaenoic acid (EPA) or combination of EPA plus docosahexaenoic acid), their dosage (higher vs. lower dose), diverse comparators (corn or mineral oil), the severity degree of the CVD risk and/or the usage of statins.5 Therefore, according to Jo et al.’s claim,5 further large-scale prospective studies are warranted to elucidate this “hype”.5...
In an initial review and meta-analysis, Rizos et al1 stated that omega-3 supplementation at low and higher dosages showed no or weak associations with cardiovascular disease (CVD) outcomes. Then, we reported more recent reviews that displayed a protective activity of omega-3 supplementation against CVD outcomes.2 Moreover, we reported that both metabolic syndrome (MetS) and Helicobacter pylori infection (Hp-I) increase the risk of cardio-cerebrovascular events, the endpoint of MetS,2 and omega-3 acids are beneficial against these disorders.2 Next, a corresponding piece commenting on our own paper by Rizos et al,3 reported that some recent data showed, for instance, low and/or high dosage of omega-3 supplementation was not associated with CVD outcomes.3 However, multiple trials continue to use low dosage of omega-3, which demonstrated substantial CVD benefits and other recent data showed that higher dosage of omega-3 (4 g/day) also induced a remarkable reduction in CVD events.4 The current contradictory findings can be attributed to several contributors including diverse types of omega-3 fatty acids (only eicosapentaenoic acid (EPA) or combination of EPA plus docosahexaenoic acid), their dosage (higher vs. lower dose), diverse comparators (corn or mineral oil), the severity degree of the CVD risk and/or the usage of statins.5 Therefore, according to Jo et al.’s claim,5 further large-scale prospective studies are warranted to elucidate this “hype”.5
Noticeably, the authors,3 commenting on the Ikezaki et al. study, claimed exactly the following: “A prospective observational study in Japan including 4014 participants showed that the dietary intake of omega-3 fatty acids was negatively associated with successful eradicarion.9” That is an incomplete - inaccurate and rather unacceptable “biased” comment, made by the authors. Actually, Ikezaki et al.6 concluded exactly as follows: “Our results indicate that higher egg and fish intake may be negatively correlated with successful H. pylori eradication therapy in H. pylori-positive subjects with gastritis and/or duodenal ulcers”,6 thereby meaning that both high cholesterol and omega-3 fatty acid intake, but not omega-3 fatty acid intake alone, may be negatively correlated with successful H. pylori eradication therapy.
In this respect, relative data suggest that mainly high cholesterol intake rather than omega-3 fatty acid intake, is negatively linked with successful H. pylori eradication regimen. For instance, a recent large-scale study reported that H. pylori infection could play a pathophysiologic role in the development of dyslipidemia, whereas H. pylori eradication may decrease the risk of dyslipidemia; significant reduction in total cholesterol was observed in the successful eradication of H. pylori arm compared to the persistent H. pylori-positive arm (P<0.001).7 A meta-analysis investigating the association between H. pylori infection and the serum lipid profile, revealed that H. pylori infection is positively associated with LDL-C, TC, and TG and negatively associated with HDL-C.8 Another recent meta-analysis also revealed that the post-H. pylori eradication HDL-C concentrations were increased while LDL-C concentrations were marginally or not influenced, and thus further investigation is necessary to clarify the effects of lipid alterations following H. pylori eradication on CVD.9 Likewise, a multicenter national study reported that H. pylori infection appears to play an independent role in the pathophysiology of the mentioned MetS; H. pylori-positive participants exhibit significantly higher body mass index, waist circumference, TC, LDL-C, and lower HDL-C, when compared with seronegative participants (P < 0.05).10 As a final example, simvastatin significantly improves H. pylori eradication rate.11
All in all, the potential effect of omega-3 supplementation on MetS and/or H. pylori-related risk of cardio-cerebrovascular events needs further evaluation before considering the introduction of low and/or high dosage of omega-3 as a possible regular regimen against cardio-cerebrovascular disorders.
References
1. Rizos EC, Markozannes G, Tsapas A, et al. Omega-3 supplementation and cardiovascular disease: formulation-based systematic review and meta-analysis with trial sequential analysis. Heart 2020;107:150-58.
2. Kountouras J, Doulberis M, Kazakos E, et al. Impact of omega-3 supplement on metabolic syndrome and/or Helicobacter pylori-related risk of cardiovascular disease. Heart 2022 Feb 9:heartjnl-2020-318776.
3. Markozannes G, Ntzani EE, Rizos EC. Correspondence on 'Impact of omega-3 supplement on metabolic syndrome and/or Helicobacter pylori-related risk of cardiovascular disease' by Kountouras et al. Heart 2022 Feb 9:heartjnl-2022-320822.
4. Elagizi A, Lavie CJ, O'Keefe E, et al. An Update on Omega-3 Polyunsaturated Fatty Acids and Cardiovascular Health. Nutrients 2021;13:204.
5. Jo SH, Han SH, Kim SH, et al. Cardiovascular effects of omega-3 fatty acids: Hope or hype? Atherosclerosis 2021;322:15-23.
6. Ikezaki H, Furusyo N, Jacques PF, et al. Higher dietary cholesterol and omega-3 fatty acid intakes are associated with a lower success rate of Helicobacter pylori eradication therapy in Japan. Am J Clin Nutr 2017;106:581-88.
7. Park Y, Kim TJ, Lee H, et al. Eradication of Helicobacter pylori infection decreases risk for dyslipidemia: A cohort study. Helicobacter 2021;26:e12783.
8. Shimamoto T, Yamamichi N, Gondo K, et al. The association of Helicobacter pylori infection with serum lipid profiles: An evaluation based on a combination of meta-analysis and a propensity score-based observational approach. PLoS One 2020;15:e0234433.
9. Watanabe J, Hamasaki M, Kotani K. The Effect of Helicobacter pylori Eradication on Lipid Levels: A Meta-Analysis. J Clin Med 2021;10:904.
10. Lim SH, Kim N, Kwon JW, et al. Positive Association Between Helicobacter pylori Infection and Metabolic Syndrome in a Korean Population: A Multicenter Nationwide Study. Dig Dis Sci 2019;64:2219-30.
11. Hassan AM, Shawky MAE, Mohammed AQ, et al. Simvastatin improves the eradication rate of Helicobacter pylori: upper Egypt experience. Infect Drug Resist 2019;12:1529-34.
Corresponding to: Jannis Kountouras, MD, PhD
Professor of Medicine
Gastroenterologist
8 Fanariou St, Byzantio 551 33,
Thessaloniki, Macedonia, Greece
Tel: +30-2310-892238, Fax: +30-2310-992794
E-mail: jannis@auth.gr, ancoratus2010@gmail.com
Contributors: JK wrote the draft of the document. AP, EV, DC, MT-C and MD critically revised it.
Funding: Dr Doulberis has received a travel grant by Gilead Sciences Switzerland Sàrl. Rest of the authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests: None declared.
Patient and public involvement: Patients and/or public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.
Patient consent for publication: This study does not involve human participants.
Prevalence and peer review: Not commissioned; internally peer reviewed
I read with great interest the report of Law et al [1]. The authors examined one-year mortality risk in 432 patients with wild-type transthyretin amyloid cardiomyopathy (wtATTR-CM) to detect useful biomarkers. The adjusted hazard ratio (HR) (95% confidence interval [CI]) of the change in N-terminal pro-B-type natriuretic peptide concentration (∆ NT-proBNP) per 500 ng/L increase for mortality was 1.04 (1.01 to 1.07). In addition, the adjusted HRs (95% CIs) of the increases in ∆ NT-proBNP of >500 ng/L, >1000 ng/L and >2000 ng/L for mortality were 1.65 (1.18-2.31), 1.92 (1.37-2.70), and 2.87 (1.93-4.27), respectively. They concluded that the change in NT-proBNP concentration during the first year was an independent predictor of mortality in patients with wtATTR-CM. I have a comment about this study.
Ochi et al. examined two-year mortality risk in 47 patients with wtATTR-CM [2], and low serum albumin (≤3.75 g/dL), elevated high-sensitivity cardiac troponin T (hs-cTnT; >0.086 ng/mL), and low left ventricular ejection fraction (LVEF; <50%) are significantly associated with mortality in patients with wtATTR-CM. According to the total number of these 3 risk factors, patients were stratified into 4 subgroups: low risk (no risk factors), intermediate-low risk (1 risk factor), intermediate-high risk (2 risk factors), and high risk (3 risk factors). The estimated two-year survival rate of patients classified as low risk, intermediate-low risk, intermediate-high r...
I read with great interest the report of Law et al [1]. The authors examined one-year mortality risk in 432 patients with wild-type transthyretin amyloid cardiomyopathy (wtATTR-CM) to detect useful biomarkers. The adjusted hazard ratio (HR) (95% confidence interval [CI]) of the change in N-terminal pro-B-type natriuretic peptide concentration (∆ NT-proBNP) per 500 ng/L increase for mortality was 1.04 (1.01 to 1.07). In addition, the adjusted HRs (95% CIs) of the increases in ∆ NT-proBNP of >500 ng/L, >1000 ng/L and >2000 ng/L for mortality were 1.65 (1.18-2.31), 1.92 (1.37-2.70), and 2.87 (1.93-4.27), respectively. They concluded that the change in NT-proBNP concentration during the first year was an independent predictor of mortality in patients with wtATTR-CM. I have a comment about this study.
Ochi et al. examined two-year mortality risk in 47 patients with wtATTR-CM [2], and low serum albumin (≤3.75 g/dL), elevated high-sensitivity cardiac troponin T (hs-cTnT; >0.086 ng/mL), and low left ventricular ejection fraction (LVEF; <50%) are significantly associated with mortality in patients with wtATTR-CM. According to the total number of these 3 risk factors, patients were stratified into 4 subgroups: low risk (no risk factors), intermediate-low risk (1 risk factor), intermediate-high risk (2 risk factors), and high risk (3 risk factors). The estimated two-year survival rate of patients classified as low risk, intermediate-low risk, intermediate-high risk, and high risk was 93%, 80%, 83%, and 11%, respectively. Although they conducted a longer follow-up period, the number of samples was limited. In addition, they used baseline data as predictors of prognosis. Regarding to the results by Law et al [1], changes in serum albumin, hs-cTnT, and LVEF did not became significant predictors for one-year mortality.
Ochi et al. used B-type natriuretic peptide concentration, which was different in clinical meaning of NT-proBNP [2]. Taken together, further studies with longer follow-up is recommended to evaluate prognosis in patients with wtATTR-CM.
REFERENCES
1 Law S, Petrie A, Chacko L, et al. Change in N-terminal pro-B-type natriuretic peptide at 1 year predicts mortality in wild-type transthyretin amyloid cardiomyopathy.. Heart 2021 May 14. doi: 10.1136/heartjnl-2021-319063
2 Ochi Y, Kubo T, Baba Y, et al. Prediction of Medium-Term Mortality in Japanese Patients With Wild-Type Transthyretin Amyloidosis. Circ Rep 2020;2:314-21.
I am one of the 95 survivors in your article having had the mustard operation in 1980 and would just like to thank everyone who took part in putting this together. I found it very usefull and interesting.
Adam Timmis gives an excellent overview of risk stratification in acute coronary syndromes and he outlines recommended management strategies.[1] We were confused however by his suggestion that "the diagnostic value of exertional ST segment depression and thallium perfusion defects are equivalent, making the treadmill more cost effective than the gamma camera". It is not clear whether the diagnostic value to which he refers is...
Adam Timmis gives an excellent overview of risk stratification in acute coronary syndromes and he outlines recommended management strategies.[1] We were confused however by his suggestion that "the diagnostic value of exertional ST segment depression and thallium perfusion defects are equivalent, making the treadmill more cost effective than the gamma camera". It is not clear whether the diagnostic value to which he refers is the diagnosis of coronary disease, the detection of residual myocardial ischaemia, or the prediction of future coronary events. He quotes a meta-analysis of Shaw and colleagues [2] who reviewed non-invasive tests in assessing the risk of coronary events after myocardial infarction, hence we presume that he intended to say that the exercise ECG is equally effective and hence more cost-effective than the gamma camera for risk stratification. We do not believe that this view is justified and we would like to expand on three points.
First, there are no formal studies of the cost-effectiveness of risk stratification after infarction, and in their absence it is not warranted to extrapolate from the effectiveness and cost of individual tests to a statement on cost-effectiveness. To do so ignores induced costs (for instance when an abnormal exercise ECG leads to angiography without subsequent intervention), it ignores the relatively high failure rate of the exercise ECG after infarction (submaximal exercise, abnormal resting ECG, etc), and it ignores the need for further investigation in the chronic phase (such as myocardial perfusion imaging if this has not already been performed). For the diagnosis of coronary artery disease, there is now powerful evidence to indicate that strategies that include myocardial perfusion imaging are more cost effective than those that do not.[3][4] Because diagnosis involves the detection of ischaemia and because persistent ischaemia after infarction is a key factor in prognosis, it is likely that formal studies of cost effectiveness of risk stratification would provide similar results.
Second, although the positive predictive value of any form of pre-discharge non-invasive testing is low,[2] Dr Timmis ignores the superior positive predictive value of perfusion imaging compared with the exercise ECG in patients who have not received thrombolysis (13% versus 9% for death and 24% versus 18% for death or reinfarction). Since the distinction between patients who have and who have not received thrombolysis is mainly the size of their infarcts, it seems to us that a test that is capable of assessing infarct size and prognosis in those with large infarcts should not be cast aside so easily. Shaw and colleagues[2] also emphasised the relatively poor quality of the studies available. For instance, three quarters of the studies were retrospective and one third reported fewer than 5 deaths, and they recognised the need for further studies to provide more reliable information. Further high quality studies are now available and we believe that the weight of evidence is that perfusion imaging is more effective than the exercise ECG for risk stratification after myocardial infarction.
Numerous studies have shown that inducible perfusion abnormalities are more common than ST segment changes on the exercise ECG.[5][6][7] This extends observations from the era before thrombolysis when an inducible thallium defect was shown to be better than the exercise ECG for detecting and localising ischaemia and for identifying multi-vessel disease. However, because thrombolysis has reduced the event rate after infarction, there are those who argue that the event rate is now so low that myocardial perfusion imaging is less valuable after infarction than it was.[5] [8] However these studies included a relatively low risk group with younger patients, preserved left ventricular function, and a low prevalence of multi-vessel disease. The higher risk patients were excluded because they mainly went straight to angiography and revascularisation and it is precisely these who would have been best identified by myocardial perfusion imaging if doubt remained after clinical assessment. In addition, selection bias was operating against perfusion imaging because when it was performed the results were used to guide intervention and hence to exclude the patient from follow-up. It is not surprising that non-invasive testing was not found to be valuable in the few remaining low risk patients.
In better designed studies there is now ample evidence that perfusion imaging is a valuable tool for risk stratification after infarction. Dakik and colleagues[7] reported that a predischarge exercise myocardial perfusion scan in patients who had received thombolysis provided incremental prognostic information over and above clinical and ejection fraction data. In contrast, none of the variables from the exercise ECG contributed to the assessment of prognosis. Similarly, Travin and colleagues[9] found that myocardial perfusion imaging within 14 days of infarction frequently revealed residual ischaemia and was better than clinical and exercise ECG variables in identifying patients at high risk. More recently, Brown and colleagues[10] reported a multi-centre trial in patients with first acute infarction. Three hundred and thirty nine patients were randomised to early (2 to 4 days) dipyridamole myocardial perfusion imaging followed by predischarge (6 to 12 days) sub-maximal exercise imaging, and 112 patients were randomised to submaximal predischarge imaging alone. The findings of the early perfusion study were not available to the responsible physicians and hence patient management was not affected. Early dipyridamole imaging was safe and was predictive of both in-hospital and late cardiac events, and it was a stronger predictor than predischarge submaximal exercise ECG or submaximal exercise perfusion imaging. This prognostic value was independent of thrombolytic status.
Third, with regard to the influence of left ventricular function on prognostic power, Mahmarian and colleagues[11] compared adenosine perfusion imaging and ejection fraction after infarction and found them to have complementary roles. They found that even patients with an ejection fraction greater than 40% were further stratified into low and high risk groups by the extent of the inducible perfusion defect. This study and the guidelines of the American College of Physicians[12] contradict Dr Timmis's recommendation that further risk stratification is not required in asymptomatic patients with an ejection fraction greater than 40%. Indeed, the ACP guidelines suggest that these are the patients in whom non-invasive risk stratification is most successful.
With the growing pressure to reduce costs but maintain quality of care, accurate risk stratification at an early stage using myocardial perfusion imaging with vasodilator stress in all but the highest risk patients could have important benefits. Low risk patients could be discharged earlier than those at a higher risk and in-hospital cardiac events might be prevented. Because of the complementary role of perfusion and functional information, it is conceivable that combined assessment of both using gated SPECT could be highly effective in routine use, particularly since left ventricular end systolic volume appears to be more powerful in prognostic terms than ejection fraction alone.
In summary, we believe that there is sufficient evidence to modify Dr Timmis's algorithm to require early myocardial perfusion imaging rather than exercise ECG in all but the highest risk patients assessed by clinical criteria, and to include patients with relatively preserved LVEF in this strategy. We predict that such an approach will be cost-effective.
S Richard Underwood, MD, FRCP, FRCR, FESC
Imperial College School of Medicine
Royal Brompton Hospital
Sydney St, London SW3 6NP
Constantinos Anagnostopoulos MD, PhD
Royal Brompton Hospital
Sydney St, London SW3 6NP
Leslee J Shaw PhD
Emory University School of Medicine
1518 Clifton Road NE, Rm638
Atlanta, Georgia 30322, USA
References
1 Timmis A. Acute coronary syndromes: risk stratification. Heart 2000;83:241-6.
2 Shaw LJ, Peterson ED, Kesler K, et al. A metaanalysis of predischarge risk stratification after acute myocardial infarction with stress electrocardiographic, myocardial perfusion and ventricular function imaging. Am J Cardiol 1996;78:1327-37.
3 Underwood SR, Godman B, Salyani S, et al. Economics of myocardial perfusion imaging in Europe: the EMPIRE study. Eur Heart J 1999;20:157-66.
4 Shaw LJ, Hachamovitch R, Berman DS, et al. The economic consequences of available diagnostic and prognostic strategies for the evaluation of stable angina patients: an observational assessment of the value of precatheterisation ischaemia. J Am Coll Cardiol 1999;33:661-9.
5 Tilkemeier PL, Guiney TE, LaRaia PJ, et al. Prognostic value of predischarge low-level exercise thallium testing after thrombolytic treatment of acute myocardial infarction. Am J Cardiol 1990;66:1203-7.
6 Haber HL, Beller GA, Watson DD, et al. Exercise thallium-201 scintigraphy after thrombolytic therapy with or without angioplasty for acute myocardial infarction. Am J Cardiol 1993;71:1257-61.
7 Dakik HA, Mahmarian JJ, Kimball KT, et al. Prognostic value of exercise 201Tl tomography in patients treated with thrombolytic therapy during acute myocardial infarction. Circulation 1996;94:2735-42.
8 Miller TD, Gersh BJ, Christian TF, et al. Limited prognostic value of thallium-201 exercise treadmill testing early after myocardial infarction in patients treated with thrombolysis. Am Heart J 1995;130:259-66.
9 Travin MI, Dessouki A, Cameron T, et al. Use of exercise technetium-99m sestamibi SPECT imaging to detect residual ischemia and for risk stratification after acute myocardial infarction. Am J Cardiol 1995;75:665-9.
10 Brown KA, Heller GV, Landin RS, et al. Early dipyridamole (99m)Tc-sestamibi single photon emission computed tomographic imaging 2 to 4 days after acute myocardial infarction predicts in-hospital and postdischarge cardiac events: comparison with submaximal exercise imaging. Circulation 1999;100:2060-6.
11 Mahmarian JJ, Mahmarian AC, Marks GF, et al. Role of adenosine thallium-201 tomography for defining long-term risk in patients after acute myocardial infarction. J Am Coll Cardiol 1995;25:1333-40.
12 Peterson ED, Shaw LJ, Kesler K, et al. Clinical guideline: part II. Risk stratification after myocardial infarction. Ann Intern Med 1997;126:561-82.
In my review on risk stratification in acute coronary syndromes,
"diagnostic value" was used conventionally to refer to the ability of
predischarge tests to predict future coronary events, particularly death
and myocardial infarction.
In response to the 3 additional points:
1. Cost-effectiveness Underwood et al are correct to caution me on
statements of cost-effectiveness. My contention was (...
In my review on risk stratification in acute coronary syndromes,
"diagnostic value" was used conventionally to refer to the ability of
predischarge tests to predict future coronary events, particularly death
and myocardial infarction.
In response to the 3 additional points:
1. Cost-effectiveness Underwood et al are correct to caution me on
statements of cost-effectiveness. My contention was (and remains) that
predischarge stress testing is usually as effective as perfusion imaging
for risk stratification and costs less. The superior quality of SPECT
compared with conventional perfusion imaging may confer some advantage
(see below) but the considerable capital costs involved will inevitably
limit its application.
2. Exercise ECG versus Perfusion Imaging Underwood et al are
incorrect to infer superiority of predischarge perfusion imaging from the
data presented in the metaanalysis of Shaw et al (1). Cardiac event rates
were higher in the studies of myocardial perfusion imaging, readily
accounting for the apparent difference between positive predictive values
for these diagnostic tests. It is for the same reason, incidentally, that
both tests appear to perform better in patients who have not received
thrombolytic therapy. Shaw emphasises in her metaanalysis that both the
exercise ECG and the radionuclide perfusion scan are blunt tools for risk
stratification and my algorithm recommends use of either test, without
expressing a preference. Underwood et al draw attention to 3 papers
comparing the exercise ECG with SPECT imaging that post-dated ShawÆs
metaanalysis (2-4). Two showed some advantage for SPECT imaging although
positive predictive values for events after hospital discharge appeared
low (specific data not provided), confirming previous reports (2-3). The
other was a small (n=71) retrospective series, in which the only
multivariate predictor of death and recurrent infarction was LV ejection
fraction (4). Only when the endpoint was extended to incorporate unstable
angina and heart failure did perfusion imaging provide independent
prognostic information. Set against the 36 studies (16,960 patients)
included in ShawÆs metaanalysis, the additional 3 selected by Underwood et
al are not overly persuasive but suggest that SPECT technology may have an
edge over the exercise ECG for risk stratification.
3. Incremental value of perfusion imaging Although one of the
studies quoted by Underwood et al found that SPECT perfusion imaging was
not independently predictive of death and recurrent infarction if LV
ejection fraction was included in the multivariate model (4), they quote
another in which incremental value was demonstrated (5). Data for stress
testing are similarly contradictory. For this reason I recommended
application of these tests (exercise ECG or perfusion scan) only in
patients with advanced LV dysfunction (LVEF <_40 in="in" whom="whom" risk="risk" is="is" greatest.="greatest." unpublished="unpublished" data="data" for="for" our="our" own="own" low="low" patients="patients" discharged="discharged" with="with" lvef="lvef"/>40% by GUSTO criteria (6)) show the estimated risk of death in
the first year is only 3.8% (2.1-5.4%) and of death and recurrent
infarction 9.8% (7.1-12.4%). The idea that these relatively low risk
survivors of acute myocardial infarction would benefit from further risk
stratification using perfusion imaging (or stress tesing) seems barely
credible. This does not of course mean that the tests should not be done
but it does mean that incautious predictions of "cost-effectiveness" may
be incorrect.
In summary, SPECT imaging may offer a small advantage over the
exercise ECG for detection of residual ischaemia in patients with acute
coronary syndromes, although it remains a blunt tool for risk
stratification. Speaking from the perspective of the coronary care unit,
there is no doubt that the availability and low cost of exercise testing
(as opposed to the relative nonavailabiltiy and high cost of SPECT
imaging) will make it a more practical solution for predischarge risk
stratification in most centres. However, perfusion imaging is a
reasonable, perhaps better, alternative in those units able to provide a
predischarge service for upward of 700 coronary patients per year, and my
algorithm allows for this.
Adam D Timmis MD, FRCP
References
1. Shaw LJ, Peterson ED, Kesler K, Hasselblad V, Califf RM. A
metaanalysis of predischarge risk stratification after acute myocardial
infarction with stress electrocardiographic, myocardial perfusion, and
ventricular function imaging. Am J Cardiol 1996;78:1327-37.
2. Travin MI, Dessouki A, Cameron T, Heller GV. Use of exercise
technetium-99m sestamibi SPECT imaging to detect residual ischemia and for
risk stratification after acute myocardial infarction Am J Cardiol
1995;75:665-9.
3. Brown KA, Heller GV, Landin RS, Shaw LJ, Beller GA, Pasquale MJ,
Haber SB. Early dipyridamole (99m)Tc-sestamibi single photon emission
computed tomographic imaging 2 to 4 days after acute myocardial infarction
predicts in-hospital and postdischarge cardiac events: comparison with
submaximal exercise imaging. Circulation 1999;100:2060-6.
4. Dakik HA, Mahmarian JJ, Kimball KT, Koutelou MG, Medrano R, Verani
MS. Prognostic value of exercise 201Tl tomography in patients treated with
thrombolytic therapy during acute myocardial infarction. Circulation.
1996;94:2735-42.
5. Mahmarian JJ, Mahmarian AC, Marks GF, Pratt CM, Verani MS. Role of
adenosine thallium-201 tomography for defining long-term risk in patients
after acute myocardial infarction. J Am Coll Cardiol 1995;25:1333-40.
While December's editorial on non-cardiac chest pain is thoughtful
and thorough,(1) there is a strange lack of emphasis on skeletal chest
pain. I am not sure if this is due to selection of patients, but I wonder
if it is the lack of a diagnostic test for skeletal pain. Since this may
involve up to 73% of patients referred with chest pain to cardiac
clinics,(2) it would seem to be of paramount importance. The author...
While December's editorial on non-cardiac chest pain is thoughtful
and thorough,(1) there is a strange lack of emphasis on skeletal chest
pain. I am not sure if this is due to selection of patients, but I wonder
if it is the lack of a diagnostic test for skeletal pain. Since this may
involve up to 73% of patients referred with chest pain to cardiac
clinics,(2) it would seem to be of paramount importance. The authors
comment on the possibility that "abnormalities" (namely oesophageal and
respiratory) may be "coincidental rather than causative" and that 60% of
patients with normal coronary angiograms and non-cardiac chest pain have a
psychiatric disorder. We all occasionally recommend angiography in
patients who cannot adapt to the pidgeonhole we offer to give more
strength to our arm, which suggests that a higher percentage of patients
with non-cardiac chest pain and psychiatric disorders will get angiography
than those who are mentally more balanced; in addition Mayou and his
colleagues have themselves demonstrated that patients who are told that
their hearts are normal but are not given a clear diagnosis remain in
trouble,(3) so it is perhaps not surprising that psychiatrists find a high
level of psychiatric disorder in these people.
In a letter to Heart,(4) I reported the reproduction of chest pain by
testing the passive range of movements and found that of 27 patients with
clinically non-cardiac chest pain one had oesophageal reflux (and
responded to treatment for this), one had costochondral joint pain and 22
had their symptoms reproduced by spinal movements. Incidentally at one
year some still had symptoms but none had been off work because of their
presenting symptoms or admitted to hospital with chest pain. This pain can
sometimes be both reproduced and relieved by intercostal nerve block (C
Davidson, personal communication). We are doing a larger study at present
but it does seem that manipulating the spine as described by Chambers et al is a
sound way of demonstrating to patient and doctor that the the pain is
mechanical. Only 7 out of 27 responded to non-steroidal anti-inflammatory
drugs; I think it is likely that postural training or (pace the
unbelievers) manipulation will do better. The hardest patients to manage
seem to be those with cardiac and skeletal pain.
The authors suggest a psychological cause if there is a situational
or phobic component to the somatic symptoms; but anxiety appears to
increase mechanical symptoms such as sciatica due to a lumbar disc,
perhaps by increased muscle tone; it is not the cause of the
symptoms.
Exercise testing is a two edged sword (did they ever make single
edged swords?). The authors mention the value of a negative test, but of
equal importance is the danger of a positive in someone with coronary
disease but non-cardiac chest pain, and the risk of intervention with no
relief of symptoms, further angiography etc.
Finally the authors suggest that for patients with "continuing
symptoms---with coexisting psychological problems" a specialist nurse who
has received additional training should be employed in the cardiac clinic
to help them. Surely if the patient has been told that they have no
cardiac disease the last place they should be followed is the cardiac
clinic whatever the actual cause of their symptoms.
I know the north-south divide involves more than house prices, but I
find it hard to believe that chest pain in Oxford or London is too
different from that in Lancashire, assuming that referral is not biased.
To demonstrate a physical cause is of tremendous importance as we are
looking at thousands of referrals per year who, if managed by their
general practitioner, would contribute to a significant drop in our
waiting lists. I suggest that some of those thousands have demonstrable
skeletal pain, and that we are missing them.
References
1 Chambers J, Bass C, Mayou R. Non-cardiac chest pain: assessment and
management. Heart 1999;82:656-7.
2 Jain D, Fluck D, Sayer JW, et al. Ability of a one-stop chest pain clinic
to identify high risk patients... J R Coll Phys Lond 1997;31:401-4.
3 Mayou R, Bryant B, Sanders D, et al. A controlled trial of cognitive
behavioural therapy for non-cardiac chest pain. Psychol Med 1997;27:1021-31.
4 Best RA. Non-cardiac chest pain: a useful physical sign? [letter] Heart 1999;81:450.
Thijssen et al. reported factors affecting the diameters of the thoracic aorta in participants (1). By using non-enhanced cardiac CT, the diameters of the ascending (AA) and descending aorta (DA) were measured. The median absolute change in diameters during follow-up with mean scan interval of 14.1 years, was 1 mm for both the AA and DA. Absolute changes per decade in AA and AD diameters were significantly larger in males than in females. Significant determinants of changes in AA diameter were age, body mass index (BMI) and diastolic blood pressure (DBP) in female, and BMI in males. In addition, significant determinants of changes in DA diameter were age, BMI, DBP, and current smoking in female, and age and BMI in males. I have a comment about the study.
There are some sex differences in significant determinants for the change of AA and AD diameters, and BMI is a common risk factor. Ferrara et al. reported that there were no effects of gender, BMI, AA diameter, aortic stiffness index, smoking habits, diabetes mellitus, and Marfan syndrome on AA tissue in patients with AA aneurysms. In contrast, aging and hypertension made the AA tissue weaker (2). The significant determinants for dilation of AA and DA diameters may not directly relate to the risk of thoracic aneurysm, and BMI management is important to prevent thoracic aorta dilations in general population.
Reference
Show More1. Thijssen CGE, Mutluer FO, van der Toorn JE, et al. Longitudinal changes of thoracic...
In the investigation recently published in “Heart”, the authors discuss the efficacy of beta blockade in treating individuals with the Takotsubo cardiomyopathy. [1] Another recent publication shows this to be a controversial topic. [2] These discussions emphasize the significance of the dose-related sensitivity of one component of three-dimensional aggregation of the ventricular cardiomyocytes, a feature which, thus far, has received little attention. Intraoperative cardio-dynamic measurements [3] have shown that the cardiomyocytes within the three-dimensional mesh that are aggregated in intruding, as opposed to tangential, fashion are statistically more sensitive to both positive and negative inotropes when given at low doses. The cardiomyocytes aggregated in transmural fashion exert a dilatory effect, in contrast to the tangential aggregates, which act exclusively to drive ventricular ejection. The different functions of the two populations indicates that the ventricular cone, as a whole, functions as an antagonistic system. [4]
Show MoreWhen the ventricular walls are hypertrophied in response to increased resistance to flow, ventricular wall thickening stretches and tilts the cardiomyocytes aggregated in transmural fashion, thus increasing the dilating forces. At the same time, of course, the transmural cardiomyocytes themselves undergo hypertrophy. This triggers a vicious circle, with both populations of cardiomyocytes undergoing hypertrophy. In this situation, however,...
I take great concern in regards to the conclusions that this and multiple other previous cardiology articles have laid claim to in regards to calcium supplementation. Many providers read these articles and tell patients to stop taking calcium, this then results in osteoporosis and fractures which also has a high mortality rate. There must be significant caution in making the conclusions that this article makes. The amount of calcium the patients were taking was quite varied between 500-2,000 mg a day, patients with bone disease need 1200 mg a day in order to maintain normal bone turnover and rebuilding by the osteoblast. There needs to be data from this study showing the poor outcome patient’s calcium supplement amounts. To insinuate that all calcium supplements are bad is not only a disservice but a detriment to our patients. Patients now have access to articles more than ever and will read this and now won’t take their calcium supplements, this means that anyone treating osteoporosis will now have to explain this and other articles. Patients are more likely to believe bad data than good data. The truth is that calcium is needed for good bone health and there is a safe amount that is not a risk to cardiac health. This article amongst others does not bring in that side of the story.
To the Editor
Show MoreWe read with interest the recent review by Griborio-Guzman AG et al [1] of the clinical presentation, diagnosis and management of cardiac myxomas. The authors highlighted that cardiac myxomas should be managed with prompt resection. Yet, the question of whether excision of an atrial myxoma qualifies as an emergency procedure remains unanswered.
In an attempt to address this question, we constructed a “best evidence topic” according to a structured protocol, as described previously [2]. A comprehensive MEDLINE literature search was conducted utilizing the PubMed interface (1966-August 2021) using the keywords: [(atrial myxoma) OR (cardiac myxoma) OR (heart myxoma)] AND [(resection) OR (removal) OR (excision)] AND [(emergency) OR (urgent) OR (immediate) OR (prompt)]. References of selected articles were then reviewed to detect relevant publications that did not come up with the original search. Two hundred and fifty-six papers were found using the reported search. From these, 11 papers were identified that provided best evidence to answer the question, all of them were single-group case-series.
In one of the earliest clinical series, Semb et al [3] emphasized that surgery should be performed as soon as the diagnosis is made, and observed that tumour fragmentation and embolization was more likely to occur when a lobulated, gelatinous and fragile myxoma was located in the central bloodstream.
Livi et al [4] reported that sudden death could...
To the Editor,
In an initial review and meta-analysis, Rizos et al1 stated that omega-3 supplementation at low and higher dosages showed no or weak associations with cardiovascular disease (CVD) outcomes. Then, we reported more recent reviews that displayed a protective activity of omega-3 supplementation against CVD outcomes.2 Moreover, we reported that both metabolic syndrome (MetS) and Helicobacter pylori infection (Hp-I) increase the risk of cardio-cerebrovascular events, the endpoint of MetS,2 and omega-3 acids are beneficial against these disorders.2 Next, a corresponding piece commenting on our own paper by Rizos et al,3 reported that some recent data showed, for instance, low and/or high dosage of omega-3 supplementation was not associated with CVD outcomes.3 However, multiple trials continue to use low dosage of omega-3, which demonstrated substantial CVD benefits and other recent data showed that higher dosage of omega-3 (4 g/day) also induced a remarkable reduction in CVD events.4 The current contradictory findings can be attributed to several contributors including diverse types of omega-3 fatty acids (only eicosapentaenoic acid (EPA) or combination of EPA plus docosahexaenoic acid), their dosage (higher vs. lower dose), diverse comparators (corn or mineral oil), the severity degree of the CVD risk and/or the usage of statins.5 Therefore, according to Jo et al.’s claim,5 further large-scale prospective studies are warranted to elucidate this “hype”.5...
Show MoreI read with great interest the report of Law et al [1]. The authors examined one-year mortality risk in 432 patients with wild-type transthyretin amyloid cardiomyopathy (wtATTR-CM) to detect useful biomarkers. The adjusted hazard ratio (HR) (95% confidence interval [CI]) of the change in N-terminal pro-B-type natriuretic peptide concentration (∆ NT-proBNP) per 500 ng/L increase for mortality was 1.04 (1.01 to 1.07). In addition, the adjusted HRs (95% CIs) of the increases in ∆ NT-proBNP of >500 ng/L, >1000 ng/L and >2000 ng/L for mortality were 1.65 (1.18-2.31), 1.92 (1.37-2.70), and 2.87 (1.93-4.27), respectively. They concluded that the change in NT-proBNP concentration during the first year was an independent predictor of mortality in patients with wtATTR-CM. I have a comment about this study.
Ochi et al. examined two-year mortality risk in 47 patients with wtATTR-CM [2], and low serum albumin (≤3.75 g/dL), elevated high-sensitivity cardiac troponin T (hs-cTnT; >0.086 ng/mL), and low left ventricular ejection fraction (LVEF; <50%) are significantly associated with mortality in patients with wtATTR-CM. According to the total number of these 3 risk factors, patients were stratified into 4 subgroups: low risk (no risk factors), intermediate-low risk (1 risk factor), intermediate-high risk (2 risk factors), and high risk (3 risk factors). The estimated two-year survival rate of patients classified as low risk, intermediate-low risk, intermediate-high r...
Show MoreDear Editor,
I am one of the 95 survivors in your article having had the mustard operation in 1980 and would just like to thank everyone who took part in putting this together. I found it very usefull and interesting.
In my review on risk stratification in acute coronary syndromes, "diagnostic value" was used conventionally to refer to the ability of predischarge tests to predict future coronary events, particularly death and myocardial infarction.
In response to the 3 additional points:
1. Cost-effectiveness Underwood et al are correct to caution me on statements of cost-effectiveness. My contention was (...
While December's editorial on non-cardiac chest pain is thoughtful and thorough,(1) there is a strange lack of emphasis on skeletal chest pain. I am not sure if this is due to selection of patients, but I wonder if it is the lack of a diagnostic test for skeletal pain. Since this may involve up to 73% of patients referred with chest pain to cardiac clinics,(2) it would seem to be of paramount importance. The author...
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