In the methods section, the formula for the Bazett correction should
be indicated as QTc = QT/(RR ^ 0.5) with RR in seconds and the Fridericia
correction formula should be indicated as QTc = QT/(RR ^ 0.333) with the
RR in seconds. This would more clearly indicate the square root and cube
root calculations used and also the relationship between the 2
corrections.
Re: Perry et al: Congratulations on your study. I have 20 years experience interviewing and assessing cardiac patients post AMI / PTCA and post CAGS and for a few years now have included a brief question at the cardiac rehabilitation entry assessment on the 'description' of the symptoms that
caused the person to seek medical attention in the first instance.
Re: Perry et al: Congratulations on your study. I have 20 years experience interviewing and assessing cardiac patients post AMI / PTCA and post CAGS and for a few years now have included a brief question at the cardiac rehabilitation entry assessment on the 'description' of the symptoms that
caused the person to seek medical attention in the first instance.
While many experience 'typical text book chest pain ', I have found a
larger number do not. These people experience various intensity of
discomfort and many have described their symptoms as in one arm or both
with no chest symptoms, or an aching in the jaw or throat or shoulders and
more than half the clients with chest symptoms describe a 'tightness'
rather than a pain.
Delay in seeking medical attention is reported to me often as 'not
relating their symptoms to being cardiac in origin' rather than any
denial. There is often a comment such as: " I didn’t really think it was my heart because I guess I expected the symptoms would be worse if it was my heart." It raises the question weather health professionals in the ambulance service and ED, GP practice and cardiac wards should change their
questioning of people about their acute symptoms from "how much chest pain
do you have?" to "do you have any discomfort or pain between the ear lobe
or belly button, front or back?”.
As part of our cardiac rehab education sessions on symptom recognition and
when to seek medical attention in both the cardiac and community groups,
we now use the patient experience as examples . This has improved
confidence and communication.
We read with great interest the article titled “Premature ventricular complexes and development of heart failure in a community-based population” by Limpitikul’s team. The study by Limpitikul et al. indicates that coupling interval heterogeneity was an independent risk factor suggests that the mechanism of premature ventricular complexes(PVC) generation may influence the risk of heart failure. The prospective study of Limpitikul et al. overcomes the referral bias of previous cross-sectional studies, but there are some questions with this study. We did not see the description of the number of Holter tests in the article, so we think that maybe all the people included in the study only performed Holter once. However, the results of a single Holter monitoring may be affected by many factors. For example, unhealthy lifestyles such as mental stress, overwork, excessive smoking, alcohol, and coffee intake can all induce PVC. In view of the fact that any factor leading to premature depolarization of ventricular muscles can be the cause of PVC, we believe that the conclusion of follow-up 11 years later based on the results of a Holter is not very credible.
We read with great interest the recent results from ESC-EORP
Registry of Pregnancy and Cardiac disease (ROPAC), concerning pregnancy.
outcomes in women with systemic right ventricle (sRV) and transposition of the
great arteries (TGA) by Tutarel et al. (1) In Tutarel et al. analysis HF was the
most frequent maternal complication (9.1%). These results are concordant
with our previous observations of 24 pregnancies of women with TGA after
atrial switch operation and matched non-pregnant controls with TGA after atrial
redirection. 2 In our series 2 women deteriorated from the functional NYHA
class I to II after the first pregnancy and one woman in her fourth pregnancy
deteriorated from class I to III. Tutarel’s results reinforce our conclusion that,
from a cardiologist’s point of view, pregnancy after the Mustard/Senning
operation was relatively well-tolerated and safe.
In ROPAC study the information on tricuspid regurgitation (TR) was collected, but was
not mandatory. Therefore Tutarel et al. concluded that dedicated studies focusing on
sRV function and TR are warranted. Our dataset provided relevant information
on sRV and TR. At baseline, all women had preserved or only mildly reduced
sRV function estimated by echocardiography before pregnancy and absent or
mild TR. There were no differences between non-pregnant matched controls
and pregnant women in sRV function, deg...
We read with great interest the recent results from ESC-EORP
Registry of Pregnancy and Cardiac disease (ROPAC), concerning pregnancy.
outcomes in women with systemic right ventricle (sRV) and transposition of the
great arteries (TGA) by Tutarel et al. (1) In Tutarel et al. analysis HF was the
most frequent maternal complication (9.1%). These results are concordant
with our previous observations of 24 pregnancies of women with TGA after
atrial switch operation and matched non-pregnant controls with TGA after atrial
redirection. 2 In our series 2 women deteriorated from the functional NYHA
class I to II after the first pregnancy and one woman in her fourth pregnancy
deteriorated from class I to III. Tutarel’s results reinforce our conclusion that,
from a cardiologist’s point of view, pregnancy after the Mustard/Senning
operation was relatively well-tolerated and safe.
In ROPAC study the information on tricuspid regurgitation (TR) was collected, but was
not mandatory. Therefore Tutarel et al. concluded that dedicated studies focusing on
sRV function and TR are warranted. Our dataset provided relevant information
on sRV and TR. At baseline, all women had preserved or only mildly reduced
sRV function estimated by echocardiography before pregnancy and absent or
mild TR. There were no differences between non-pregnant matched controls
and pregnant women in sRV function, degree of TR, at the last follow-up visit
(mean follow-up period 80 ± 57 months for pregnant group versus 84 ± 49
months for nulliparous controls (P=NS). Significant deterioration of tricuspid
regurgitation (from mild to moderate) was observed in one pregnant woman
(after fourth pregnancy) and in one nulliparous woman. Increase in TR severity
was not accompanied by a significant reduction of sRV systolic function evaluated by
echocardiography.
References
1. Tutarel O, Baris L, Budts W, et al
Pregnancy outcomes in women with a systemic right ventricle and transposition of the great arteries results from the ESC-EORP Registry of Pregnancy and Cardiac disease (ROPAC)
Heart Published Online First: 28 April 2021. doi: 10.1136/heartjnl-2020-318685
2. Lipczynska M, Szymanski P, Trojnarska O, et al. Pregnancy in women with complete transposition of the great arteries following the atrial switch procedure. A study from three of the largest Adult Congenital Heart Disease centers in Poland, The Journal of Maternal-Fetal & Neonatal Medicine, DOI:10.1080/14767058.2016.1177821
The observation that SGLT-2 inhibitors might favourably modify the natural history of heart failure with preserved ejection fraction(HFpEF) and might also mitigate the risk of onset of atrial fibrillation(AF)(1) might have, as its rationale, the fact that both disorders are characterised by the presence of myocardial fibrosis, the latter a probable consequence of an obesity-related proinflammatory cascade which is potentially amenable to mitigation by SGLT-2 inhibitor therapy.
Adipose tissue is a source of proinflammatory cytokines such as tumor necrosis factor-alpha(TNF-alpha), Interleukin 1(IL-1), and Interleukin 6(IL-6), all three of which are secreted in increased amounts in response to obesity(2). Accordingly the presence of myocardial fibrosis either in the atria or in the ventricles might be the end result of a proinflammatory cascade originating in adipose tissue. Atrial fibrosis has been documented in obese subjects(body mass index > 30 kg/metre squared) who do not have AF(3) and and also in subjects who have established AF(4). In the former category there are, arguably, some individuals who will subsequently develop AF.
The relevance of SGLT-2 inhibitors to the association of myocardial fibrosis and either HFpEF or AF has emerged from the study which showed an anti-inflammatory effect of SGLT2 inhibitor therapy in the normoglycemic rabbit model of atherosclerosis. In that study the inflammatory content of atherosclerotic plaqu...
The observation that SGLT-2 inhibitors might favourably modify the natural history of heart failure with preserved ejection fraction(HFpEF) and might also mitigate the risk of onset of atrial fibrillation(AF)(1) might have, as its rationale, the fact that both disorders are characterised by the presence of myocardial fibrosis, the latter a probable consequence of an obesity-related proinflammatory cascade which is potentially amenable to mitigation by SGLT-2 inhibitor therapy.
Adipose tissue is a source of proinflammatory cytokines such as tumor necrosis factor-alpha(TNF-alpha), Interleukin 1(IL-1), and Interleukin 6(IL-6), all three of which are secreted in increased amounts in response to obesity(2). Accordingly the presence of myocardial fibrosis either in the atria or in the ventricles might be the end result of a proinflammatory cascade originating in adipose tissue. Atrial fibrosis has been documented in obese subjects(body mass index > 30 kg/metre squared) who do not have AF(3) and and also in subjects who have established AF(4). In the former category there are, arguably, some individuals who will subsequently develop AF.
The relevance of SGLT-2 inhibitors to the association of myocardial fibrosis and either HFpEF or AF has emerged from the study which showed an anti-inflammatory effect of SGLT2 inhibitor therapy in the normoglycemic rabbit model of atherosclerosis. In that study the inflammatory content of atherosclerotic plaques was assessed by immunostaining for TNF-alpha, IL-1 Beta , and IL-6. The content of all three cytokines was significantly decreased in the subgroup of rabbits pretreated with SGLT-2 inhibitors(5), implying a role for SGLT-2 inhibitors in the amelioration of the proinflammatory cascade that culminates in the formation of atherosclerotic plaques. The corollary might, arguably, be amelioration, by SGLT-2 inhibitors, of the proinflammatory cascade that culminates in the occurrence of myocardial fibrosis in HFpEF and AF.
I have no funding and no conflict of interest
References
(1) Gulsin GS., GrahampBrown MPM., Squire IB et al
Benefits of sodium glucose cotransporter 2 inhibitors across the spectrum of cardiovascular diseases
Heart 2021
Article in Press
(2)Lee H., Lee IS., Choue R
Obesity, inflammation an diet
Pediatric Gastroenterology, Hepatology & Nutrition 2013;16:143-152
(3)Siebermair J., Suksaranjit P., McGann CJ et al
Atrial fibrosis in non-atrial fibrillation individuals and prediction of atrial fibrillation by use of late gadolinium enhancement magnetic resonance imaging
J Cardiovasc Electrophysiol 2019;30:550-556
(4) Gai P., Marrouche NF
Magnetic resonance imaging of atrial fibrosis : redefining atrial fibrillation to ma syndrome
Eur Heart J 2017;38:14-19
(5) Lee S-G., Lee S-J., Lee J-J et al
Anti-inflammatory effect for atherosclerosis progression by sodium-glucose cotransporter 2 (SGLT-2) inhibitor in a normoglycemic rabbit model
Korean Circulatory Journal 2020;50:443-457
I read the report of Naylor-Wardle et al.1 The authors reviewed the effect of socioeconomic status (SES) on all-cause and cardiovascular disease in the COVID-19 era. Combination of CVD morbidity and COVID-19 infection relate to severity of disease and poor prognosis. A lower SES and ethnic minority both contribute to the increased mortality and CVD incidence, which is accelerated by COVID-19 infection, especially in the vulnerable elderly populations. They also made an emphasis that lifestyle factors such as tobacco, alcohol, high-fat and salt content food might be more exposed in populations with lower SES, and I want to present some information about this review.
First, Machado et al. conducted a long-term retrospective cohort study to evaluate the association between midlife wealth mobility and risk of CVD events in adults of 50 years or older.2 Higher initial wealth was significantly associated with lower cardiovascular risk. In addition, participants who experienced upward and downward wealth mobility significantly presented lower and higher hazards of a subsequent non-fatal CVD event or CVD death, respectively. This means that the inverse relationship between SES and CVD are also observed in a changing state of SES midlife populations. In the era of COVID-19 pandemic, SES in people might be changed in response to social status. Taken together, health risk assessment should be conducted prospectively by considering...
I read the report of Naylor-Wardle et al.1 The authors reviewed the effect of socioeconomic status (SES) on all-cause and cardiovascular disease in the COVID-19 era. Combination of CVD morbidity and COVID-19 infection relate to severity of disease and poor prognosis. A lower SES and ethnic minority both contribute to the increased mortality and CVD incidence, which is accelerated by COVID-19 infection, especially in the vulnerable elderly populations. They also made an emphasis that lifestyle factors such as tobacco, alcohol, high-fat and salt content food might be more exposed in populations with lower SES, and I want to present some information about this review.
First, Machado et al. conducted a long-term retrospective cohort study to evaluate the association between midlife wealth mobility and risk of CVD events in adults of 50 years or older.2 Higher initial wealth was significantly associated with lower cardiovascular risk. In addition, participants who experienced upward and downward wealth mobility significantly presented lower and higher hazards of a subsequent non-fatal CVD event or CVD death, respectively. This means that the inverse relationship between SES and CVD are also observed in a changing state of SES midlife populations. In the era of COVID-19 pandemic, SES in people might be changed in response to social status. Taken together, health risk assessment should be conducted prospectively by considering the change in SES.
Second, Makaroun et al. reported that low wealth was significantly associated with death and disability in the United States and England,3 and the significant relationship existed from middle into later life in adults. Although ethnic difference should be evaluated comprehensively, there was no generation gap on the inverse association between SES and mortality/disability. Combinations of unhealthy lifestyle factors might be strongly associated with CVD events and mortality, and SES would affect the association. Namely, SES would have interactions with lifestyle factors and also moderate the association between lifestyle factor combinations and adverse health outcomes. In any case, a meta-analysis of prospective studies is needed to evaluate the inter-relationship among SES, lifestyle factors and CVD events.4
Finally, De Bacquer et al. precisely evaluated the relationship between SES and cardiovascular risk factors.5 The adjusted odds ratios (ORs) (95% confidence intervals [CIs]) of low SES for smoking in men, physical activity in men and women, obesity in men and women were 1.63 (1.37 to 1.95), 1.51 (1.28 to 1.78), 1.77 (1.32 to 2.37), 1.28 (1.11 to 1.49) and 1.65 (1.30 to 2.10), respectively. In addition, the adjusted OR (95% CI) of low SES for raised blood pressure in men and women were 1.24 (1.07 to 1.43) and 1.31 (1.03 to 1.67), respectively. Furthermore, there was also a significant relationship between SES and markers of well-being. These data present that preclinical stage of CVD is closely related to low SES and social determinants for CVD may be relatively large. In the era of COVID-19, there are increasing needs for considering socioeconomic factors for CVD evens.
REFERENCES
Naylor-Wardle J, Rowland B, Kunadian V. Socioeconomic status and cardiovascular health in the COVID-19 pandemic. Heart 2021;107:358-65.
Machado S, Sumarsono A, Vaduganathan M. Midlife wealth mobility and long-term cardiovascular health. JAMA Cardiol 2021 Jun 30:e212056. doi: 10.1001/jamacardio.2021.2056. [Epub ahead of print]
Makaroun LK, Brown RT, Diaz-Ramirez LG, et al. Wealth-associated disparities in death and disability in the United States and England. JAMA Intern Med 2017;177:1745-53.
Foster H, Polz P, Mair F, et al. Understanding the influence of socioeconomic status on the association between combinations of lifestyle factors and adverse health outcomes: a systematic review protocol. BMJ Open 2021;11:e042212.
De Bacquer D, van de Luitgaarden IAT, De Smedt D, et al. Socioeconomic characteristics of patients with coronary heart disease in relation to their cardiovascular risk profile. Heart 2021;107:799-806.
Sodium-glucose co-transporter 2 (SGLT2) inhibitor therapy is a specific mode of anti-diabetic strategy that significantly improves cardiovascular outcomes (1). The recently published article by Joshi SS, et al (1) has focused on beneficial effects of SGLT2 inhibitors in the setting of heart failure (HF). We fully agree that complex cellular mechanisms, beyond diuresis (1), seem to underlie pleitrophic actions of these agents. More specifically, it also seems likely that SGLT2 inhibitors might potentiate favorable effects of certain metabolic agents including cellular anti-ischemics (and vice versa) in diabetic patients with cardiovascular disease. Accordingly, combination of SGLT2 inhibitors with cellular anti-ischemic regimens might have important implications in these patients:
It is well known that free fatty a...
Sodium-glucose co-transporter 2 (SGLT2) inhibitor therapy is a specific mode of anti-diabetic strategy that significantly improves cardiovascular outcomes (1). The recently published article by Joshi SS, et al (1) has focused on beneficial effects of SGLT2 inhibitors in the setting of heart failure (HF). We fully agree that complex cellular mechanisms, beyond diuresis (1), seem to underlie pleitrophic actions of these agents. More specifically, it also seems likely that SGLT2 inhibitors might potentiate favorable effects of certain metabolic agents including cellular anti-ischemics (and vice versa) in diabetic patients with cardiovascular disease. Accordingly, combination of SGLT2 inhibitors with cellular anti-ischemic regimens might have important implications in these patients:
It is well known that free fatty acids (FFAs) serve as the major energy source in myocardium under physiological conditions (1). However, a significant shift to oxidation of more energy-efficient substrates (including glucose and ketone bodies) usually takes place in the setting of myocardial ischemia and/or failure (2). Moreover, this shift is expected to be even more pronounced under certain medications including cellular anti-ischemics (trimetazidine, etc.) that exert their actions largely through inhibition of FFA oxidation (3). In a recent meta-analysis comprising diabetic patients, trimetazidine was demonstrated to exert favorable effects including improvement in left ventricular systolic functions, myocardial ischemic episodes and serum glucose parameters (fasting glucose and HbA1C), etc. largely attributable to its metabolic, anti-oxidant and anti-hyperglycemic effects in these patients (3). However, impaired myocardial uptake of glucose in diabetic patients (1-3) potentially hinders maximum therapeutic benefits of cellular anti-ischemics during periods of heightened metabolic demand. This signifies the need for alternative energy-efficient substrates (including ketone bodies) in diabetic patients receiving cellular anti-ischemics.
In this context, SGLT2 inhibitors provide sufficient amounts of circulating ketone bodies (1) that seem to maximize actions of cellular anti-ischemics on myocardial energetics in diabetic patients. Moreover, hyperketonemia associated with SGLT2 inhibitors (1) might also prevent excessive uptake of FFAs (a reactive phenomenon predisposing to diabetic cardiomyopathy due to lipotoxicity (2)) potentially associated with the use of cellular anti-ischemics in diabetic patients. On the other hand, cellular anti-ischemics might possibly heighten favorable impact of SGLT2 inhibitors mostly through their metabolic actions (increased insulin sensitivity due to translocation of GLUT4 ,etc. (3)) and anti-oxidant features (that might reverse myocardial remodeling (3)). Accordingly, combined use of certain metabolic agents including SGLT2 inhibitors, dichloroacetate, perhexiline, trimetazidine, etc. , was previously suggested as a potential strategy to combat failing myocardium (yet; with no recommendation of a particular combination) (4). In this regard, combination of SGLT2 inhibitors and trimetazidine seems to be a promising option (due to the mutually complementary actions of these agents).
In summary, concomitant use of cellular anti-ischemics and SGLT2 inhibitors might result in a synergistic therapeutic benefit in diabetic patients with cardiovascular disease (HF and coronary syndromes). However, this needs to be tested in clinical trials.
Conflict of Interest: None
References:
1- Joshi SS, Singh T, Newby DE, Singh J. Sodium-glucose co-transporter 2 inhibitor therapy: mechanisms of action in heart failure. Heart. 2021 Feb 26:heartjnl-2020-318060. doi: 10.1136/heartjnl-2020-318060. Epub ahead of print. PMID: 33637556
2- García-Ropero Á, Vargas-Delgado AP, Santos-Gallego CG, Badimon JJ. Inhibition of Sodium Glucose Cotransporters Improves Cardiac Performance. Int J Mol Sci. 2019; 20(13): 3289. doi: 10.3390/ijms20133289. PMID: 31277431; PMCID: PMC6651487.
3- Lin Y, Wang ZL, Yan M, Zhu FY, Duan Y, Sun ZQ. Effect of Trimetazidine on Diabetic Patients with Coronary Heart Diseases: A Meta-Analysis of Randomized, Controlled Trials. Chin Med Sci J. 2020; 35(3): 226-238.
4- Hamilton DJ. Metabolic Recovery of the Failing Heart: Emerging Therapeutic Options. Methodist Debakey Cardiovasc J. 2017; 13(1): 25-28. doi: 10.14797/mdcj-13-1-25. PMID: 28413579; PMCID: PMC5385791.
Dear Editor,
we thank you for your recent Editorial (1) that gives a balanced and useful view of the use of anti-interleukin1 agents for the treatment of recurrent pericarditis (2). As it is common, the authors conclude that “however, larger RCT data are required for further validation of the efficacy and safety of these novel medications in the treatment of recurrent pericarditis.” Here there is a technical issue, that sometimes may be not well appreciated. One of the first step in planning a RCT is to calculate the sample size. The point is that RCT that will randomize subjects to anti-IL 1 agents vs placebo will never be large, and will always include a small number of subjects, as compared to sample sizes common in other fields of cardiology, simply given the large treatment effect; for this reason is not ethical to randomize higher number of subjects. The calculated sample sizes are relatively small only due to the expected extremely high efficacy: e.g. the per protocol calculated sample sizes were 20 subjects in the AIRTRIP trial (3) and 56 in the RHAPSOSY trial (4). In practice we will never have “large” RCT on this topic, because these agents are expected to be so effective that the calculated sample sizes will be always small.
1. Anthony C, Collier P. Anti-interleukin-1 for recurrent pericarditis; maybe a fix (but prior studies do not really mix). Heart. 2021 May 10:heartjnl-2021-319282. doi: 10.1136/heartjnl-2021-319282. Online ahead of print.
Dear Editor,
we thank you for your recent Editorial (1) that gives a balanced and useful view of the use of anti-interleukin1 agents for the treatment of recurrent pericarditis (2). As it is common, the authors conclude that “however, larger RCT data are required for further validation of the efficacy and safety of these novel medications in the treatment of recurrent pericarditis.” Here there is a technical issue, that sometimes may be not well appreciated. One of the first step in planning a RCT is to calculate the sample size. The point is that RCT that will randomize subjects to anti-IL 1 agents vs placebo will never be large, and will always include a small number of subjects, as compared to sample sizes common in other fields of cardiology, simply given the large treatment effect; for this reason is not ethical to randomize higher number of subjects. The calculated sample sizes are relatively small only due to the expected extremely high efficacy: e.g. the per protocol calculated sample sizes were 20 subjects in the AIRTRIP trial (3) and 56 in the RHAPSOSY trial (4). In practice we will never have “large” RCT on this topic, because these agents are expected to be so effective that the calculated sample sizes will be always small.
1. Anthony C, Collier P. Anti-interleukin-1 for recurrent pericarditis; maybe a fix (but prior studies do not really mix). Heart. 2021 May 10:heartjnl-2021-319282. doi: 10.1136/heartjnl-2021-319282. Online ahead of print.
2. Imazio M, Andreis A, Piroli F, et al. Anti-interleukin1 agents for the treatment of recurrent pericarditis: a systematic review and meta-analysis.Heart 2021. doi:10.1136/heartjnl-2020-318869. [Epub ahead of print: 18 Mar 2021].
3. Brucato A, Imazio M, Gattorno M, et al. Effect of Anakinra on recurrent pericarditis among patients with colchicine resistance and corticosteroid dependence: the AIRTRIP randomized clinical trial. JAMA 2016;316:1906–12.
4. Klein AL, Imazio M, Cremer P, et al. Phase 3 trial of interleukin-1 trap rilonacept in recurrent pericarditis. N Engl J Med 2021;384:31–41.
In an excellent analysis published in the recent issue of the journal, “Heart” Lau et al. investigated the long-term clinic outcomes of patients with Takotsubo syndrome (TTS) in a large cohort. The results demonstrated that increasing age, male gender, diabetes mellitus, pulmonary disease and chronic kidney disease were associated with a higher risk of recurrence or death1. We wish to highlight a few points relevant to the article.
Núñez-Gil et al reported their findings whilst categorizing patients with TTS based upon proposed etiology. Individuals with idiopathic or emotional triggers were considered as having the primary disease, whereas those with likely physical causative factors were deemed to have a secondary form of the pathology. The analysis of both groups revealed a disparity in clinical outcomes; patients with underlying physical triggers displayed higher risk of both short and long-term adverse events 2. Similar findings have also been reported in other studies 3.
Prior published data has theorized that a history of diabetes mellitus may be relatively protective against developed of TTS possibly due to an ameliorated sympathetic response when compared to non-diabetics due to involvement related to diabetic neuropathy 4. Comparatively poorer outcomes in diabetic TTS patients as seen in this study may be possibly explained by the fact that these diabetic patients may have been overwhelmingly sicker to generate enough catecho...
In an excellent analysis published in the recent issue of the journal, “Heart” Lau et al. investigated the long-term clinic outcomes of patients with Takotsubo syndrome (TTS) in a large cohort. The results demonstrated that increasing age, male gender, diabetes mellitus, pulmonary disease and chronic kidney disease were associated with a higher risk of recurrence or death1. We wish to highlight a few points relevant to the article.
Núñez-Gil et al reported their findings whilst categorizing patients with TTS based upon proposed etiology. Individuals with idiopathic or emotional triggers were considered as having the primary disease, whereas those with likely physical causative factors were deemed to have a secondary form of the pathology. The analysis of both groups revealed a disparity in clinical outcomes; patients with underlying physical triggers displayed higher risk of both short and long-term adverse events 2. Similar findings have also been reported in other studies 3.
Prior published data has theorized that a history of diabetes mellitus may be relatively protective against developed of TTS possibly due to an ameliorated sympathetic response when compared to non-diabetics due to involvement related to diabetic neuropathy 4. Comparatively poorer outcomes in diabetic TTS patients as seen in this study may be possibly explained by the fact that these diabetic patients may have been overwhelmingly sicker to generate enough catecholaminic surge to have TTS 1.
The present analysis is similar to previous data and suggests that patients with underlying physical triggers may be at a disproportionate risk for unfavorable clinical outcomes 1, 4. We continue to suggest that patients with TTS be categorized and separately analyzed based upon primary or secondary disease etiology to allow for a better understanding of these two distinct entities and its related risk prognostication 4. We are also intrigued by the role of diabetes and TTS related adverse events and look forward to further research highlighting this association.
References
1. Lau C, Chiu S, Nayak R, Lin B, Lee MS. Survival and risk of recurrence of takotsubo syndrome. Heart. 2021 Jan 8:heartjnl-2020-318028. doi: 10.1136/heartjnl-2020-318028. Epub ahead of print. PMID: 33419884.
2. Núñez-Gil IJ, Almendro-Delia M, Andrés M, Sionis A, Martin A, Bastante T, Córdoba-Soriano JG, Linares JA, González Sucarrats S, Sánchez-Grande-Flecha A, Fabregat-Andrés O, Pérez B, Escudier-Villa JM, Martin-Reyes R, Pérez-Castellanos A, Rueda Sobella F, Cambeiro C, Piqueras-Flores J, Vidal-Perez R, Bodí V, García de la Villa B, Corbí-Pascua M, Biagioni C, Mejía-Rentería HD, Feltes G, Barrabés J; RETAKO investigators. Secondary forms of Takotsubo cardiomyopathy: A whole different prognosis. Eur Heart J Acute Cardiovasc Care. 2016 Aug;5(4):308-16. doi: 10.1177/2048872615589512. Epub 2015 Jun 4. PMID: 26045512.
3. Chhabra L, Sareen P, Mwansa V, Khalid N. Mortality in Takotsubo cardiomyopathy should also be accounted based on predisposing etiology. Ann Noninvasive Electrocardiol. 2019 Jul;24(4):e12664. doi: 10.1111/anec.12664. Epub 2019 Jun 2. PMID: 31155779; PMCID: PMC6931614.
4. Khalid N, Ahmad SA, Umer A, Chhabra L. Role of Microcirculatory Disturbances and Diabetic Autonomic Neuropathy in Takotsubo Cardiomyopathy. Crit Care Med. 2015 Nov;43(11):e527. doi: 10.1097/CCM.0000000000001183. PMID: 26468716.
For the sake of completeness, the cardiac manifestations of rheumatological disorders documented by Sen et al(1) also ought to include bacterial as well as mycobacterial and fungal infections which invade either the pericardium or the myocardium in patients with rheumatological disorders. The following are some examples:-
Suppurative pericarditis attributable to Staphylococcus aureus was documented by Huskisson et al in one of the patients in their series of 12 rheumatiod arthritis(RA) patients with severe , unusual and recurrent infections(2). A massive tuberculous plericardial effusion was documented in a 60 year old man with long-standing RA who was not taking any immunosuppressive medication(3).
Staphylococcal pericarditis was reported in a 52 year old woman with systemic lupus erythematosus(SLE) who was on prednisolone(4). Tuberculous pericarditis coexisted with SLE in 3 patients who were participants in a series consisting of 72 SLE patients with coexisting active tuberculosis infection(5).
Eosinophilic granulomatosis with polyangiitis was the underlying rheumatological disorder in a 60 year old woman who died after experiencing complications of congestive heart failure. Autopsy examination revealed invasive myocarditis secondary to Aspergillus fumigatus infection as well as multiple myocardial abscesses(6).
Comment
In the context of multisystem rheumatological disease the expectation is that the occurrence of pericarditis a...
For the sake of completeness, the cardiac manifestations of rheumatological disorders documented by Sen et al(1) also ought to include bacterial as well as mycobacterial and fungal infections which invade either the pericardium or the myocardium in patients with rheumatological disorders. The following are some examples:-
Suppurative pericarditis attributable to Staphylococcus aureus was documented by Huskisson et al in one of the patients in their series of 12 rheumatiod arthritis(RA) patients with severe , unusual and recurrent infections(2). A massive tuberculous plericardial effusion was documented in a 60 year old man with long-standing RA who was not taking any immunosuppressive medication(3).
Staphylococcal pericarditis was reported in a 52 year old woman with systemic lupus erythematosus(SLE) who was on prednisolone(4). Tuberculous pericarditis coexisted with SLE in 3 patients who were participants in a series consisting of 72 SLE patients with coexisting active tuberculosis infection(5).
Eosinophilic granulomatosis with polyangiitis was the underlying rheumatological disorder in a 60 year old woman who died after experiencing complications of congestive heart failure. Autopsy examination revealed invasive myocarditis secondary to Aspergillus fumigatus infection as well as multiple myocardial abscesses(6).
Comment
In the context of multisystem rheumatological disease the expectation is that the occurrence of pericarditis and/or myocarditis will be attributable to the prevailing rheumatological disorder. However, in the occasional case, those complications are attributable to bacterial, mycobacterial, or fungal co-infection. Clinicians should be vigilant for that eventuality.
References
(1)Sen G., Gordon P., Sado DM
Cardiac manifestations of rheumatological disease: a synopsis for the cardiologist
Heart Epub ahead of print
(2)Huskisson EC., Hart FD
Severe, unusual, and recurrent infections in rheumatoid arthritis
Ann Rheum Dis 1972;31:118-121
(3) Habib S., Akhter P., Razzak S et al
Presentation of tuberculosis as isolated massive pericardial effusion in a patient with rheumatiod arthritis
J Pak Med Assoc 2012;62:65-67
(4) Knodell RG., Manders SJ
Staphylococcus pericarditis in a patient with Systemic Lupus Erythematosus
CHEST 1974;65:103-105
(5)Torrez-Gonzalez P., Romero-Diaz J., Cervera-Hernandez ME et al
Tuberculosis and systemic lupus erythematosus : a case-control study in Mexico City
Clinical Rheumatology 2018;37:2095-2102
(6)Bullis SS., Krywanczyk A., Hale AJ
Aspergillosis myocarditis in the immunocompromised host
ID cases 2019;17:e00567
Dear Editor,
In the methods section, the formula for the Bazett correction should be indicated as QTc = QT/(RR ^ 0.5) with RR in seconds and the Fridericia correction formula should be indicated as QTc = QT/(RR ^ 0.333) with the RR in seconds. This would more clearly indicate the square root and cube root calculations used and also the relationship between the 2 corrections.
Dear Editor,
Re: Perry et al: Congratulations on your study. I have 20 years experience interviewing and assessing cardiac patients post AMI / PTCA and post CAGS and for a few years now have included a brief question at the cardiac rehabilitation entry assessment on the 'description' of the symptoms that caused the person to seek medical attention in the first instance.
While many experience 'typical text book...
We read with great interest the article titled “Premature ventricular complexes and development of heart failure in a community-based population” by Limpitikul’s team. The study by Limpitikul et al. indicates that coupling interval heterogeneity was an independent risk factor suggests that the mechanism of premature ventricular complexes(PVC) generation may influence the risk of heart failure. The prospective study of Limpitikul et al. overcomes the referral bias of previous cross-sectional studies, but there are some questions with this study. We did not see the description of the number of Holter tests in the article, so we think that maybe all the people included in the study only performed Holter once. However, the results of a single Holter monitoring may be affected by many factors. For example, unhealthy lifestyles such as mental stress, overwork, excessive smoking, alcohol, and coffee intake can all induce PVC. In view of the fact that any factor leading to premature depolarization of ventricular muscles can be the cause of PVC, we believe that the conclusion of follow-up 11 years later based on the results of a Holter is not very credible.
We read with great interest the recent results from ESC-EORP
Show MoreRegistry of Pregnancy and Cardiac disease (ROPAC), concerning pregnancy.
outcomes in women with systemic right ventricle (sRV) and transposition of the
great arteries (TGA) by Tutarel et al. (1) In Tutarel et al. analysis HF was the
most frequent maternal complication (9.1%). These results are concordant
with our previous observations of 24 pregnancies of women with TGA after
atrial switch operation and matched non-pregnant controls with TGA after atrial
redirection. 2 In our series 2 women deteriorated from the functional NYHA
class I to II after the first pregnancy and one woman in her fourth pregnancy
deteriorated from class I to III. Tutarel’s results reinforce our conclusion that,
from a cardiologist’s point of view, pregnancy after the Mustard/Senning
operation was relatively well-tolerated and safe.
In ROPAC study the information on tricuspid regurgitation (TR) was collected, but was
not mandatory. Therefore Tutarel et al. concluded that dedicated studies focusing on
sRV function and TR are warranted. Our dataset provided relevant information
on sRV and TR. At baseline, all women had preserved or only mildly reduced
sRV function estimated by echocardiography before pregnancy and absent or
mild TR. There were no differences between non-pregnant matched controls
and pregnant women in sRV function, deg...
The observation that SGLT-2 inhibitors might favourably modify the natural history of heart failure with preserved ejection fraction(HFpEF) and might also mitigate the risk of onset of atrial fibrillation(AF)(1) might have, as its rationale, the fact that both disorders are characterised by the presence of myocardial fibrosis, the latter a probable consequence of an obesity-related proinflammatory cascade which is potentially amenable to mitigation by SGLT-2 inhibitor therapy.
Show MoreAdipose tissue is a source of proinflammatory cytokines such as tumor necrosis factor-alpha(TNF-alpha), Interleukin 1(IL-1), and Interleukin 6(IL-6), all three of which are secreted in increased amounts in response to obesity(2). Accordingly the presence of myocardial fibrosis either in the atria or in the ventricles might be the end result of a proinflammatory cascade originating in adipose tissue. Atrial fibrosis has been documented in obese subjects(body mass index > 30 kg/metre squared) who do not have AF(3) and and also in subjects who have established AF(4). In the former category there are, arguably, some individuals who will subsequently develop AF.
The relevance of SGLT-2 inhibitors to the association of myocardial fibrosis and either HFpEF or AF has emerged from the study which showed an anti-inflammatory effect of SGLT2 inhibitor therapy in the normoglycemic rabbit model of atherosclerosis. In that study the inflammatory content of atherosclerotic plaqu...
I read the report of Naylor-Wardle et al.1 The authors reviewed the effect of socioeconomic status (SES) on all-cause and cardiovascular disease in the COVID-19 era. Combination of CVD morbidity and COVID-19 infection relate to severity of disease and poor prognosis. A lower SES and ethnic minority both contribute to the increased mortality and CVD incidence, which is accelerated by COVID-19 infection, especially in the vulnerable elderly populations. They also made an emphasis that lifestyle factors such as tobacco, alcohol, high-fat and salt content food might be more exposed in populations with lower SES, and I want to present some information about this review.
First, Machado et al. conducted a long-term retrospective cohort study to evaluate the association between midlife wealth mobility and risk of CVD events in adults of 50 years or older.2 Higher initial wealth was significantly associated with lower cardiovascular risk. In addition, participants who experienced upward and downward wealth mobility significantly presented lower and higher hazards of a subsequent non-fatal CVD event or CVD death, respectively. This means that the inverse relationship between SES and CVD are also observed in a changing state of SES midlife populations. In the era of COVID-19 pandemic, SES in people might be changed in response to social status. Taken together, health risk assessment should be conducted prospectively by considering...
Show MoreSodium-glucose co-transporter 2 inhibitors with cellular anti-ischemics: A favorable combination in diabetic patients with cardiovascular disease
Kenan YALTA, MD a
Ugur OZKAN, MD a
Tulin YALTA, MD b
a,TrakyaUniversity, CardiologyDepartment, Edirne, TURKEY
b,TrakyaUniversity, Pathology Department, Edirne, TURKEY
Corresponding Author: Kenan YALTA Trakya University, CardiologyDepartment, Edirne, TURKEY
Email- kyalta@gmail.com, akenanyalta@trakya.edu.tr Phone: 00905056579856
Sodium-glucose co-transporter 2 (SGLT2) inhibitor therapy is a specific mode of anti-diabetic strategy that significantly improves cardiovascular outcomes (1). The recently published article by Joshi SS, et al (1) has focused on beneficial effects of SGLT2 inhibitors in the setting of heart failure (HF). We fully agree that complex cellular mechanisms, beyond diuresis (1), seem to underlie pleitrophic actions of these agents. More specifically, it also seems likely that SGLT2 inhibitors might potentiate favorable effects of certain metabolic agents including cellular anti-ischemics (and vice versa) in diabetic patients with cardiovascular disease. Accordingly, combination of SGLT2 inhibitors with cellular anti-ischemic regimens might have important implications in these patients:
Show MoreIt is well known that free fatty a...
Dear Editor,
we thank you for your recent Editorial (1) that gives a balanced and useful view of the use of anti-interleukin1 agents for the treatment of recurrent pericarditis (2). As it is common, the authors conclude that “however, larger RCT data are required for further validation of the efficacy and safety of these novel medications in the treatment of recurrent pericarditis.” Here there is a technical issue, that sometimes may be not well appreciated. One of the first step in planning a RCT is to calculate the sample size. The point is that RCT that will randomize subjects to anti-IL 1 agents vs placebo will never be large, and will always include a small number of subjects, as compared to sample sizes common in other fields of cardiology, simply given the large treatment effect; for this reason is not ethical to randomize higher number of subjects. The calculated sample sizes are relatively small only due to the expected extremely high efficacy: e.g. the per protocol calculated sample sizes were 20 subjects in the AIRTRIP trial (3) and 56 in the RHAPSOSY trial (4). In practice we will never have “large” RCT on this topic, because these agents are expected to be so effective that the calculated sample sizes will be always small.
1. Anthony C, Collier P. Anti-interleukin-1 for recurrent pericarditis; maybe a fix (but prior studies do not really mix). Heart. 2021 May 10:heartjnl-2021-319282. doi: 10.1136/heartjnl-2021-319282. Online ahead of print.
...Show MoreTo the Editor,
In an excellent analysis published in the recent issue of the journal, “Heart” Lau et al. investigated the long-term clinic outcomes of patients with Takotsubo syndrome (TTS) in a large cohort. The results demonstrated that increasing age, male gender, diabetes mellitus, pulmonary disease and chronic kidney disease were associated with a higher risk of recurrence or death1. We wish to highlight a few points relevant to the article.
Núñez-Gil et al reported their findings whilst categorizing patients with TTS based upon proposed etiology. Individuals with idiopathic or emotional triggers were considered as having the primary disease, whereas those with likely physical causative factors were deemed to have a secondary form of the pathology. The analysis of both groups revealed a disparity in clinical outcomes; patients with underlying physical triggers displayed higher risk of both short and long-term adverse events 2. Similar findings have also been reported in other studies 3.
Prior published data has theorized that a history of diabetes mellitus may be relatively protective against developed of TTS possibly due to an ameliorated sympathetic response when compared to non-diabetics due to involvement related to diabetic neuropathy 4. Comparatively poorer outcomes in diabetic TTS patients as seen in this study may be possibly explained by the fact that these diabetic patients may have been overwhelmingly sicker to generate enough catecho...
Show MoreFor the sake of completeness, the cardiac manifestations of rheumatological disorders documented by Sen et al(1) also ought to include bacterial as well as mycobacterial and fungal infections which invade either the pericardium or the myocardium in patients with rheumatological disorders. The following are some examples:-
Show MoreSuppurative pericarditis attributable to Staphylococcus aureus was documented by Huskisson et al in one of the patients in their series of 12 rheumatiod arthritis(RA) patients with severe , unusual and recurrent infections(2). A massive tuberculous plericardial effusion was documented in a 60 year old man with long-standing RA who was not taking any immunosuppressive medication(3).
Staphylococcal pericarditis was reported in a 52 year old woman with systemic lupus erythematosus(SLE) who was on prednisolone(4). Tuberculous pericarditis coexisted with SLE in 3 patients who were participants in a series consisting of 72 SLE patients with coexisting active tuberculosis infection(5).
Eosinophilic granulomatosis with polyangiitis was the underlying rheumatological disorder in a 60 year old woman who died after experiencing complications of congestive heart failure. Autopsy examination revealed invasive myocarditis secondary to Aspergillus fumigatus infection as well as multiple myocardial abscesses(6).
Comment
In the context of multisystem rheumatological disease the expectation is that the occurrence of pericarditis a...
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