We use cookies to improve our service and to tailor our content and advertising to you.More infoYou can manage your cookie settings via your browser at any time. To learn more about how we use cookies, please see our cookies policy.
The recommendation that combined antiplatelet and new oral anticoagulant(NOAC) therapy should rely on the lowest approved NOAC dose effective for stroke prevention(1) is one which favours low-dose edoxaban instead of either dabigatran, rivaroxaban, or apixaban, when reduction of risk of gastrointestinal(GIT) bleeding is taken into account. In a review of clinical experience of bleeding associated with NOACs(dabigatran, rivaroxaban, apixaban, and edoxaban) versus warfarin in nonvalvular atrial fibrillation(NVAF), edoxaban 30 mg/day was the only antithrombotic agent associated with significantly(p < 0.001) lower risk of GIT bleeding than warfarin(Hazard Ratio: 0.67;95% Confidence Interval 0.53 to 0.83). For apixaban and for dabigatran 110 mg BID, the risk of GIT bleeding was comparable with the risk associated with warfarin use. For rivaroxaban and for dabigatran 150 mg BID the risk of GIT haemorrhage was significantly higher(P < 0.0001, and p < 0.001, respectively) than the GIT bleeding risk associated with warfarin(2).
In a study where 92.2% of 5301 NVAF users of antiplatelet agents were prescribed a NOAC in combination with only one antiplatelet agent vs 86.3% of 9106 NVAF users of antiplatelet agents who were prescribed warfarin with only one antiplatelet agent , concomitant antiplatelet and NOAC use was associated with significantly lower risk of intracranial bleeding than concomitant antiplatelet and warfarin use(HR 0.68, 95% CI, 0.51 to 0.91). Ne...
The recommendation that combined antiplatelet and new oral anticoagulant(NOAC) therapy should rely on the lowest approved NOAC dose effective for stroke prevention(1) is one which favours low-dose edoxaban instead of either dabigatran, rivaroxaban, or apixaban, when reduction of risk of gastrointestinal(GIT) bleeding is taken into account. In a review of clinical experience of bleeding associated with NOACs(dabigatran, rivaroxaban, apixaban, and edoxaban) versus warfarin in nonvalvular atrial fibrillation(NVAF), edoxaban 30 mg/day was the only antithrombotic agent associated with significantly(p < 0.001) lower risk of GIT bleeding than warfarin(Hazard Ratio: 0.67;95% Confidence Interval 0.53 to 0.83). For apixaban and for dabigatran 110 mg BID, the risk of GIT bleeding was comparable with the risk associated with warfarin use. For rivaroxaban and for dabigatran 150 mg BID the risk of GIT haemorrhage was significantly higher(P < 0.0001, and p < 0.001, respectively) than the GIT bleeding risk associated with warfarin(2).
In a study where 92.2% of 5301 NVAF users of antiplatelet agents were prescribed a NOAC in combination with only one antiplatelet agent vs 86.3% of 9106 NVAF users of antiplatelet agents who were prescribed warfarin with only one antiplatelet agent , concomitant antiplatelet and NOAC use was associated with significantly lower risk of intracranial bleeding than concomitant antiplatelet and warfarin use(HR 0.68, 95% CI, 0.51 to 0.91). Nevertheless, risk of GIT bleeding was comparable(HR 1,08, 95% CI, 0.81 to 1.45)(3).
Given the fact that VKA therapy is associated with greater risk of intracranial bleeding than NOAC therapy, not only in the absence of concomitant antiplatelet drug use(2), but also in the context of combined anticoagulant and only one antiplatelet agent (3), the safest use of triple antithrombotic therapy(TAT) appears to be one which involves either low-dose edoxaban, low-dose dabigatran or apixaban so as to optimise mitigation of the risk of gastrointestinal bleeding..
Although PIONEER AF-PCI was a TAT study which documented significantly(p < 0.001) lower rates of clinically significant bleeding in recipients of TAT involving low dose rivaroxaban than in recipients of TA involving warfarin that study was not powered to evaluate non inferiority of the low-dose rivaroxaban regime to the warfarin regime for thromboprophylaxis against NVAF-related stroke(4). Future trials should now optimise the advantage that the sole use of low-dose edoxaban enjoys over sole use of other NOACs in mitigating the risk of both intracranial and GIT bleeding, by exploring the possibility that the universal inclusion of the 30 mg/day edoxaban dose (irrespective of renal function and body weight), in a TAT regime might be non inferior to a TAT regime that involves warfarin, with regard to thromboprophylaxis against NVAF-related stroke. .
I have no funding and no conflict of interest
References
(1) Capodano D
Triple antithrombotic therapy after ACS and PCI in patients on chronic oral anticoagulation Update
Heart 2018;104:1976-1983
(2) Eikelboom J., Meril G
Bleeding with direct oral anticoagulants vs warfarin: Clinical experience
Am J Med 2016;129:S33-S40
(3)Douros A., Renoux X., Yin H et al
Concomitant use of direct oral anticoagulants with antiplatelet agents and the risk of major bleeding in patients with nonvalvular atrial fibrillation
Am J Med 2018;DOI.org/10.1016/amjmed 2018.10.008
(4) Gibson CM., Mehran R., Bode C et al
Prevention of bleeding in patients with atrial fibrillation undergoing PCI
N Engl J Med 2016;375:2423-2434
Given the fact that constrictive pericarditis is an eminently reversible cause of congestive heart failure(CHF) its timely clinical recognition deserved special mention in the recent review of epidemiology of pericardial diseases in Africa(1). Timely recognition and treatment might, arguably, mitigate the risk of perioperative mortality which is currently of the order of 12.5% to 14%, given the fact that this adverse statistic is principally generated by patients who come to operation in New York Heart Association functional class III and IV(2)(3). Accordingly, what needs to be done is to educate doctors and medical students to identify stigmata which differentiate CP from "run of the mill" CHF so as to expedite early referral of suspected CP to tertiary centres for definitive diagnosis and, hence, timely pericardiectomy.
According to Little and Freeman, in the typical case of CP, "there will be marked jugular venous distension, hepatic congestion, ascites, and peripheral oedema, while the lungs remain clear"(3). Consequently, on the basis of their series of 30 patients, Evans and Jackson observed that "the presence of distended neck veins in a patient who is able to lie comfortably in the recumbent posture is characteristic of the disease"(4). The jugular venous pressure(JVP) response to a diagnostic trial of diuretic therapy may also be of diagnostic significance(5)(6). In CP, the typical response is that the JVP remains persisten...
Given the fact that constrictive pericarditis is an eminently reversible cause of congestive heart failure(CHF) its timely clinical recognition deserved special mention in the recent review of epidemiology of pericardial diseases in Africa(1). Timely recognition and treatment might, arguably, mitigate the risk of perioperative mortality which is currently of the order of 12.5% to 14%, given the fact that this adverse statistic is principally generated by patients who come to operation in New York Heart Association functional class III and IV(2)(3). Accordingly, what needs to be done is to educate doctors and medical students to identify stigmata which differentiate CP from "run of the mill" CHF so as to expedite early referral of suspected CP to tertiary centres for definitive diagnosis and, hence, timely pericardiectomy.
According to Little and Freeman, in the typical case of CP, "there will be marked jugular venous distension, hepatic congestion, ascites, and peripheral oedema, while the lungs remain clear"(3). Consequently, on the basis of their series of 30 patients, Evans and Jackson observed that "the presence of distended neck veins in a patient who is able to lie comfortably in the recumbent posture is characteristic of the disease"(4). The jugular venous pressure(JVP) response to a diagnostic trial of diuretic therapy may also be of diagnostic significance(5)(6). In CP, the typical response is that the JVP remains persistently in spite of resolution of peripheral oedema(5)(6), even when this is accompanied by weight loss(5). At the very least, patients who exhibit those stigmata should have chest x-ray to detect pericardial calcification. If the index of suspicion for CP still persists, the next step should be computed tomography of the thorax to detect pericardial thickening.
In developed countries delay in the clinical recognition of CP is common(7), but this diagnostic lapse can be excused on the basis of the rarity of CP in those societies. In the African context, however, where CP is more prevalent, preventable diagnostic delay is inexcusable.
I have no conflict of interest and no funding
References
(1) Noubiap JJ., Agbor VN., Ndoadoumgue AL et al
Epidemiology of pericardial disease in Africa: A sytematic review
Heart 10th November 2018;Doi 10.1136/heartjnl2018-313922
(2) Yangni-Angate K., Tanauh Y., Meneas C et al
Surgical experience on chronic constricitve pericarditis in African setting: review of 35 years experience in Cote d'Ivorie
Cardiovasc Diagn Ther 2016,6(Suppl 1):S13-S19
(3)Mutyaba AK., Balkaran S., Cloete R et al
Constrictive pericarditis requiring pericardiectomy at Groote Schuur Hospital Capetown, South Africa: Cuases and perioperative outcomes in the HIV era(1990-2012)
The Journal of Thoracic and Cardiovascular surgery 2014;148:3058-3065
(3)Little WC., Freeman GL
Pericardial disease
Circulation 2006;113:1622-1632
(4) Evans W., Jackson F
Constrictive pericarditis
British Heart Journal 1952:14:53-69
(5)Conti CR., Friesinger GC
Chronic constrictive pericarditis; clinical and laboratory findings in 11 case
Johns Hopkins Med J 1967;120:262-274
(6) Chambliss JR., Jaruszewski EJ., Brofman BL., Martin JF., Feil H
Chronic cardiac compression(Chronic constrictive pericarditis)
A critical study of sixty one operated cases with follow up
Circulation 1951;4:816-835
(7) Marshall A., Ring N., Lewis T
Constrictive pericarditis: lessons from the past five years experience in the South West Cardiothoracic centre
Clinical Medicine 2006;6:592-597
We read with interest the article by Rusingiza et al (1)and report our experience from Northern Sri Lanka, a Low Middle Income Country (LMIC). Sri Lanka had invested heavily in free education and healthcare with demonstrably high literacy rates and positive health indices (2). However, the focus of the healthcare related investment has been in the secondary and tertiary care institutions, whilst primary care systems remain poorly developed. Northern Sri Lanka had been further impacted adversely by three decades of civil strife.
We report our experience in the management of post-valvular surgery patients at the Jaffna Teaching Hospital, the only tertiary referral centre for the region. Improvements in socioeconomic conditions has resulted in a decline in the incidence of rheumatic heart disease in Sri Lanka which accounted for only 0.34% of all deaths in 2017 (3). Concurrently, established patients receiving prosthetic heart valves has increased mainly due to improving access to surgical facilities. Unfortunately, Northern Sri Lanka had been without facilities for cardiac surgery for three decades leaving patients to access facilities elsewhere in the country. Post-surgery follow-up occurred primarily in Jaffna and a few other secondary care hospitals in the region. Unlike in the Rwandan study, most of our patients received parenteral penicillin prophylaxis thereby enhancing compliance and were fitted with metallic rather than bioprosthetic valves, thereby necessitat...
We read with interest the article by Rusingiza et al (1)and report our experience from Northern Sri Lanka, a Low Middle Income Country (LMIC). Sri Lanka had invested heavily in free education and healthcare with demonstrably high literacy rates and positive health indices (2). However, the focus of the healthcare related investment has been in the secondary and tertiary care institutions, whilst primary care systems remain poorly developed. Northern Sri Lanka had been further impacted adversely by three decades of civil strife.
We report our experience in the management of post-valvular surgery patients at the Jaffna Teaching Hospital, the only tertiary referral centre for the region. Improvements in socioeconomic conditions has resulted in a decline in the incidence of rheumatic heart disease in Sri Lanka which accounted for only 0.34% of all deaths in 2017 (3). Concurrently, established patients receiving prosthetic heart valves has increased mainly due to improving access to surgical facilities. Unfortunately, Northern Sri Lanka had been without facilities for cardiac surgery for three decades leaving patients to access facilities elsewhere in the country. Post-surgery follow-up occurred primarily in Jaffna and a few other secondary care hospitals in the region. Unlike in the Rwandan study, most of our patients received parenteral penicillin prophylaxis thereby enhancing compliance and were fitted with metallic rather than bioprosthetic valves, thereby necessitating the need for long-term monitoring on warfarin, the only available anticoagulant in the state sector in Sri Lanka. This need, together with the increase in valvular surgery following the recent development of cardiac surgery in Jaffna, further emphasizes the urgent need for managing these patients in integrated primary care setups closer to their homes.
It is encouraging that Sri Lanka has now recognized the urgency to develop the primary care infrastructure, driven by the emerging epidemic in Non-Communicable Diseases. The lesson from Rwanda is of relevance to countries like Sri Lanka and will decrease the overloading of secondary and tertiary institutions with overall reductions in the cost of healthcare.
References:
1. Rusingiza EK, El-Khatib Z, Hedt-Gauthier B et al. Outcomes for patients with rheumatic heart disease after cardiac surgery followed at rural district hospitals in Rwanda. Heart. 2018; 104:1707-1714
2. WHOAnnualReport2012.http://www.who.int/kobe_centre/publications/annual_report2012_en.pdf.
3. https://www.worldlifeexpectancy.com/sri-lanka-rheumatic-heart-disease
To the Editor, we read with great interest the article by Ntiloudi et al[1], describing hospitalization for heart failure (HF) as a powerful predictor of mortality among adults with pulmonary hypertension related to congenital heart disease (PH-ACHD). Although pulmonary arterial hypertension (PAH) targeted therapy has improved their survival, long-term complications such as HF hospitalization commonly occurred, and dismal prognosis with a mortality rate of 18.5% deeply broke our heart, thus requiring earlier diagnosis, risk stratification and therapeutic intervention.
Hospitalization for HF, a sign of clinical worsening, is associated with poor outcomes and generally used as one of composite endpoints in PAH[2], Ntiloudi et al stated nearly one-quarter of patients were hospitalized for HF, and they encountered a ninefold increased mortality risk compared to those not-hospitalized, since NYHA functional class III/IV raised a tenfold risk of death, its combination with HF hospitalization may better predict outcomes. A previous study[3] reported 29% patients with idiopathic and associated PAH were hospitalized for acute right heart failure at least once during a 39.1-month follow up, and those with hospitalizations had worse NYHA functional class, inferior right ventricle function, lower six minute walk test (6MWT) distance and worse outcomes defined by death/transplant (67% vs 33%). These two findings indicated a potential role of HF hospitalization for identifying...
To the Editor, we read with great interest the article by Ntiloudi et al[1], describing hospitalization for heart failure (HF) as a powerful predictor of mortality among adults with pulmonary hypertension related to congenital heart disease (PH-ACHD). Although pulmonary arterial hypertension (PAH) targeted therapy has improved their survival, long-term complications such as HF hospitalization commonly occurred, and dismal prognosis with a mortality rate of 18.5% deeply broke our heart, thus requiring earlier diagnosis, risk stratification and therapeutic intervention.
Hospitalization for HF, a sign of clinical worsening, is associated with poor outcomes and generally used as one of composite endpoints in PAH[2], Ntiloudi et al stated nearly one-quarter of patients were hospitalized for HF, and they encountered a ninefold increased mortality risk compared to those not-hospitalized, since NYHA functional class III/IV raised a tenfold risk of death, its combination with HF hospitalization may better predict outcomes. A previous study[3] reported 29% patients with idiopathic and associated PAH were hospitalized for acute right heart failure at least once during a 39.1-month follow up, and those with hospitalizations had worse NYHA functional class, inferior right ventricle function, lower six minute walk test (6MWT) distance and worse outcomes defined by death/transplant (67% vs 33%). These two findings indicated a potential role of HF hospitalization for identifying higher risk population in PAH.
Although multiple factors were reported to predict mortality in PAH-CHD, clinical risk stratification remains a challenge. Current multivariable risk stratification model encompassing age, shunt location, pericardial effusion, 6MWT distance and oxygen saturation facilitates outcome evaluation for adult patients with Eisenmenger syndrome[4]. Older age unanimously correlated with worse prognosis[1, 4], yet shunt location did not have a finger in the pie[1], which might be explained by small sample size and heterogeneous cohort. Hospitalization for heart failure is a promising risk stratification tool for PH-ACHD and could be considered in the above multivariable model.
As mentioned by Ntiloudi et al, essential factors such as BNP level, functional capacity, echocardiographic and hemodynamic data were unavailable, thus further larger multicenter studies regarding all aforementioned factors are encouraged to validate the role of hospitalization for HF in risk stratification and the suggested prognostic model.
Qi Jin, Qin Luo, Zhihui Zhao, Zhihong Liu
Center for Pulmonary Vascular Diseases, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China
QJ and QL contributed equally.
Correspondence to Professor Zhihong Liu, Center for Pulmonary Vascular Diseases, Fuwai Hospital, 167 Beilishi Road, Xicheng District, Beijing 100037, China; zhihongliufuwai@163.com
Contributors QJ and QL read the article and wrote the letter. ZZ read the article and revised the letter. ZL provided the concept and revised the manuscript. All authors approved the final version.
Competing interests None declared.
REFERENCES
1. Ntiloudi D, Apostolopoulou S, Vasiliadis K, Frogoudaki A, Tzifa A, Ntellos C, Brili S, Manginas A, Pitsis A, Kolios M et al: Hospitalisations for heart failure predict mortality in pulmonary hypertension related to congenital heart disease. Heart 2018; pii: heartjnl-2018-313613. Doi: 10.1136/heartjnl-2018-313613.
2. Takatsuki S, Nakayama T, Ikehara S, Matsuura H, Ivy DD, Saji T: Pulmonary Arterial Capacitance Index Is a Strong Predictor for Adverse Outcome in Children with Idiopathic and Heritable Pulmonary Arterial Hypertension. J Pediatr 2017; 180:75-79 e72.
3. Talavera MLL, Favaloro LE, Caneva JO, Klein F, Boughen RP, Osses JM, Bertolotti AM, Favaloro RR: Prognostic value of right heart failure hospitalizations in pulmonary arterial hypertension. Eur J Heart Fail 2014; 16:294-294.
4. Kempny A: Prognostication in PAH–CHD. In: Pulmonary Hypertension in Adult Congenital Heart Disease. Edited by Dimopoulos K, Diller G-P. Cham: Springer International Publishing; 2017: 315-328.
There was significantly higher usage of both loop diuretics and aldosterone antagonist in the group with persistent hyponatraemia. Is it possible that one of the clinical manifestation of RV dysfunction, i.e peripheral oedema, led to an increased use of diuretic in this group and hence hyponatraemia as a complication of this treatment? Over diuresis in this scenario leads to activation of the RAAS which in turn worsens pulmonary hypertension and tricuspid regurgitation. The consequence of this is worsening peripheral oedema and the tendency to increase the diuretic dose.Hyponatraemia therefore may not be an independent predictor of outcome as stated.
We read with great interest the article by Elias et al (1) regarding the longer term clinical outcomes from the EXPLORE trial. The authors are to be congratulated for conducting this important study to address the optimal management of patients presenting with a concurrent CTO in a non-infarct related artery (non-IRA) during a STEMI. The results at 1 year are similar to those in the initial 4 month outcome (2), with no difference in the primary endpoints of cardiac MRI determined LVEF or LVEDV in either CTO-PCI and CTO-No PCI groups. At a median of 3.9 years, there was no difference in long term MACE, although an apparent increase in cardiovascular mortality (6% vs 1%, p=0.02).
Whilst this important study adds to the much needed literature on randomised studies related to PCI of CTOs, the results should be interpreted with caution. Firstly, large scale contemporaneous studies in CTO PCI have had procedural success rates in the region of 90% (3), whilst in EXPLORE (2) this rate was considerably lower, at 73% by core laboratory. This suggests either a more anatomically complex subset of patients, or else attempts by non-dedicated CTO PCI operators, both of which affect the interpretation of the intention to treat population.
Furthermore, the mortality data should be reviewed with care. At 12 months, there were 4 cardiovascular deaths (2.7%) in the CTO PCI group, with no deaths in the CTO-No PCI groups. These rates are significantly lower compared with other t...
We read with great interest the article by Elias et al (1) regarding the longer term clinical outcomes from the EXPLORE trial. The authors are to be congratulated for conducting this important study to address the optimal management of patients presenting with a concurrent CTO in a non-infarct related artery (non-IRA) during a STEMI. The results at 1 year are similar to those in the initial 4 month outcome (2), with no difference in the primary endpoints of cardiac MRI determined LVEF or LVEDV in either CTO-PCI and CTO-No PCI groups. At a median of 3.9 years, there was no difference in long term MACE, although an apparent increase in cardiovascular mortality (6% vs 1%, p=0.02).
Whilst this important study adds to the much needed literature on randomised studies related to PCI of CTOs, the results should be interpreted with caution. Firstly, large scale contemporaneous studies in CTO PCI have had procedural success rates in the region of 90% (3), whilst in EXPLORE (2) this rate was considerably lower, at 73% by core laboratory. This suggests either a more anatomically complex subset of patients, or else attempts by non-dedicated CTO PCI operators, both of which affect the interpretation of the intention to treat population.
Furthermore, the mortality data should be reviewed with care. At 12 months, there were 4 cardiovascular deaths (2.7%) in the CTO PCI group, with no deaths in the CTO-No PCI groups. These rates are significantly lower compared with other trials in the modern era of primary-PCI for STEMI, such as TOTAL (4) (3.7% 12 month cardiovascular mortality in 10,064 patients and 10.8% in patients with concurrent CTO in non-IRA) and HORIZONS-AMI (5) (2.9% 12 month mortality in 3,602 patients). This lower than expected event rate may affect the ability to detect differences between treatment arms. Furthermore, the mechanism of the deaths in the CTO-PCI group at 12 months was stent thrombosis (ST) in all 4 cases. Whilst drug eluting stents were used for all CTO-PCI and the majority of culprit STEMI lesions, along with mandated dual antiplatelet therapy for all patients, the overall rate of probable or definite ST was relatively high at 5.6%, in contrast to TOTAL4 and HORIZONS-AMI5, which had a 1.9% and 3% ST rate at 12 months. Given the CTO PCI procedure was conducted at operator discretion it would be interesting to note whether intravascular imaging was used, as IVUS guided CTO PCI has been shown to reduce rates of ST. Clarification on this would be important, and may help to explain the high rate of ST.
24.0% of patients in the CTO-No PCI group underwent either CTO PCI or CABG within 1 year. Clearly this high cross over rate has implications for data analysis, and further underlines the inherent issues with attempting to conduct a meaningful CTO PCI trial. Finally, this study was addressing the issue of early complete revascularisation in patients with a STEMI and concurrent CTO. We have previously shown (6) with landmark analysis, that even beyond 1 month, the presence of a CTO in patients with a STEMI is associated with significantly poorer prognosis above and beyond that of multi-vessel disease. Clearly, the “double jeopardy” with a CTO of a non-infarct related artery and STEMI results in a greater territory of ischaemic myocardium with an early rate of cardiogenic shock and mortality. However, whether a staged PCI procedure after allowing recovery of the myocardium would result in improved outcomes should be an area of ongoing research.
References
1. Elias J, van Dongen IM, Ramunddal T, Laanmets P, Eriksen E, Meuwissen M, Michels HR, Bax M, Ioanes D, Suttorp MJ, Strauss BH, Barbato E, Marques KM, Claessen B, Hirsch A, van der Schaaf RJ, Tijssen JGP, Henriques JPS, Hoebers LP and investigators E. Long-term impact of chronic total occlusion recanalisation in patients with ST-elevation myocardial infarction. Heart. 2018;104:1432-1438.
2. Henriques JP, Hoebers LP, Ramunddal T, Laanmets P, Eriksen E, Bax M, Ioanes D, Suttorp MJ, Strauss BH, Barbato E, Nijveldt R, van Rossum AC, Marques KM, Elias J, van Dongen IM, Claessen BE, Tijssen JG, van der Schaaf RJ and Investigators ET. Percutaneous Intervention for Concurrent Chronic Total Occlusions in Patients With STEMI: The EXPLORE Trial. J Am Coll Cardiol. 2016;68:1622-1632.
3. Park S-J. DECISION-CTO: Optimal Medical Therapy With or Without Stenting For Coronary Chronic Total Occlusion. American College of Cardiology Annual Scientific Session (ACC 2017). 2017.
4. Jolly SS, Cairns JA, Yusuf S, Rokoss MJ, Gao P, Meeks B, Kedev S, Stankovic G, Moreno R, Gershlick A, Chowdhary S, Lavi S, Niemela K, Bernat I, Cantor WJ, Cheema AN, Steg PG, Welsh RC, Sheth T, Bertrand OF, Avezum A, Bhindi R, Natarajan MK, Horak D, Leung RC, Kassam S, Rao SV, El-Omar M, Mehta SR, Velianou JL, Pancholy S, Dzavik V and Investigators T. Outcomes after thrombus aspiration for ST elevation myocardial infarction: 1-year follow-up of the prospective randomised TOTAL trial. Lancet. 2016;387:127-35.
5. Mehran R, Lansky AJ, Witzenbichler B, Guagliumi G, Peruga JZ, Brodie BR, Dudek D, Kornowski R, Hartmann F, Gersh BJ, Pocock SJ, Wong SC, Nikolsky E, Gambone L, Vandertie L, Parise H, Dangas GD, Stone GW and Investigators H-AT. Bivalirudin in patients undergoing primary angioplasty for acute myocardial infarction (HORIZONS-AMI): 1-year results of a randomised controlled trial. Lancet. 2009;374:1149-59.
6. Allahwala UK, Jolly SS, Dzavik V, Cairns JA, Kedev S, Balasubramanian K, Stankovic G, Moreno R, Valettas N, Bertrand O, Lavi S, Velianou JL, Sheth T, Meeks B, Brilakis ES and Bhindi R. The Presence of a CTO in a Non-Infarct-Related Artery During a STEMI Treated With Contemporary Primary PCI Is Associated With Increased Rates of Early and Late Cardiovascular Morbidity and Mortality: The CTO-TOTAL Substudy. JACC Cardiovasc Interv. 2018;11:709-711.
We thank dr. Katsouras for his response to our long-term EXPLORE manuscript (1). We agree that in the ST-segment elevation (STEMI) population the presence of collaterals to the concurrent chronic total occlusion (CTO) is of prognostic relevance. We previously reported in 413 consecutive STEMI patients with a CTO that the presence of well-developed collaterals to the CTO compared to poorly developed collaterals was associated with improved outcome. We also assessed the influence of the collateral origin on survival, as collaterals coming distally from the culprit lesion are (partially) blocked during the acute phase of STEMI. In 16% of the patients the collaterals originated directly or distal from the culprit lesion and these patients had a lower survival compared to the patients in whom the collaterals were not blocked during STEMI (2).
In the EXPLORE trial patients with well-developed collaterals to the CTO had a significantly better left ventricular (LV) function at 4 months follow-up. Nonetheless, we did not find a significant treatment effect of CTO-PCI on global LV function nor on clinical outcome in patients with poorly developed nor with well-developed collaterals (3). On a regional level we found that the recovery of segmental wall thickening of the dysfunctional CTO myocardium was better in patients with well-developed collaterals. However, no significant interaction of collateral quality on the effect of CTO PCI was found (4). In EXPLORE there were 34 p...
We thank dr. Katsouras for his response to our long-term EXPLORE manuscript (1). We agree that in the ST-segment elevation (STEMI) population the presence of collaterals to the concurrent chronic total occlusion (CTO) is of prognostic relevance. We previously reported in 413 consecutive STEMI patients with a CTO that the presence of well-developed collaterals to the CTO compared to poorly developed collaterals was associated with improved outcome. We also assessed the influence of the collateral origin on survival, as collaterals coming distally from the culprit lesion are (partially) blocked during the acute phase of STEMI. In 16% of the patients the collaterals originated directly or distal from the culprit lesion and these patients had a lower survival compared to the patients in whom the collaterals were not blocked during STEMI (2).
In the EXPLORE trial patients with well-developed collaterals to the CTO had a significantly better left ventricular (LV) function at 4 months follow-up. Nonetheless, we did not find a significant treatment effect of CTO-PCI on global LV function nor on clinical outcome in patients with poorly developed nor with well-developed collaterals (3). On a regional level we found that the recovery of segmental wall thickening of the dysfunctional CTO myocardium was better in patients with well-developed collaterals. However, no significant interaction of collateral quality on the effect of CTO PCI was found (4). In EXPLORE there were 34 patients (11%) with no visible collaterals or collaterals originating from the IRA occluded during STEMI. These patients had a significantly lower LVEF (38% versus 45%, p=0.001) and a higher LVEDV (226ml versus 213ml, p=0.37) at 4 months follow-up. Long-term MACE rates were also numerically higher in this group (20% versus 12%, Log-rank p=0.21). Mortality rates were not different between both groups (9.4% versus 9.3%, Log-rank p=0.40). We did not find an effect of CTO-PCI on LV function nor on clinical outcome in the patients with collaterals blocked during STEMI nor in patients with present collaterals.
Therefore, data regarding the value of the collateral circulation are conflicting and their exact role remains controversial. Further CTO research should focus more on the collateral circulation to determine whether collaterals should be of influence on treatment strategies or whether they are just unmodifiable markers of prognosis in these complex patients.
References:
1. Elias J, van Dongen IM, Ramunddal T, et al. Long-term impact of chronic total occlusion recanalisation in patients with ST-elevation myocardial infarction. Heart 2018 doi: 10.1136/heartjnl-2017-312698
2. Elias J, Hoebers LPC, van Dongen IM, et al. Impact of Collateral Circulation on Survival in ST-Segment Elevation Myocardial Infarction Patients Undergoing Primary Percutaneous Coronary Intervention With a Concomitant Chronic Total Occlusion. JACC Cardiovasc Interv 2017;10(9):906-14. doi: 10.1016/j.jcin.2017.01.026
3. Van Dongen IM, Elias J, Van Houwelingen KG, et al. P5156Impact of collateral filling on LVF and survival in STEMI patients with a concomitant CTO. An explorative subanalysis of the EXPLORE trial. European Heart Journal 2017;38(suppl_1):ehx493.P5156-ehx493.P56. doi: 10.1093/eurheartj/ehx493.P5156
4. Elias J, van Dongen IM, Hoebers LP, et al. Improved recovery of regional left ventricular function after PCI of chronic total occlusion in STEMI patients: a cardiovascular magnetic resonance study of the randomized controlled EXPLORE trial. J Cardiovasc Magn Reson 2017;19(1):53. doi: 10.1186/s12968-017-0369-z
I read with great interest the paper by Elias et al regarding the mid-term and long-term clinical outcome of the Evaluating Xience and left ventricular function in Percutaneous Coronary Interventions on occlusiOns afteR ST elevation myocardial infarction (EXPLORE) trial. [1] The authors are to be congratulated for this detailed analysis evaluating the effect of chronic total occlusions – percutaneous coronary intervention (CTO-PCI) compared with CTO-No PCI on clinical outcome, left ventricular function and angina status in patients with ST elevation myocardial infarction (STEMI) with a concurrent CTO. The message of their study is that early CTO-PCI in patients with STEMI presenting with a concurrent CTO during primary PCI should not be performed routinely.
The authors also analysed the study population combined and found higher long-term mortality in patients who were older (>60 years) (11% vs 3%; HR 3.74; 95% CI 1.37 to 10.21; P=0.01), who had diabetes (15% vs 6%; HR 2.94; 95% CI 1.19 to 7.30; P=0.02), had a higher left ventricular enddiastolic volume at baseline (12% vs 1%; HR 13.04; 95% CI 1.70 to 100.30; P=0.01) and who had a high SYNTAX score (10% vs 4%; HR 2.50; 95% CI 1.01 to 6.20; P=0.048). They also stated that cardiac death was more frequent in the CTO-PCI arm (6.0% vs 1.0%, P=0.02) with no difference in all-cause mortality. However, it is known that a major prognostic factor in STEMI patients with a concurrent CTO is the presence of collateral feeding...
I read with great interest the paper by Elias et al regarding the mid-term and long-term clinical outcome of the Evaluating Xience and left ventricular function in Percutaneous Coronary Interventions on occlusiOns afteR ST elevation myocardial infarction (EXPLORE) trial. [1] The authors are to be congratulated for this detailed analysis evaluating the effect of chronic total occlusions – percutaneous coronary intervention (CTO-PCI) compared with CTO-No PCI on clinical outcome, left ventricular function and angina status in patients with ST elevation myocardial infarction (STEMI) with a concurrent CTO. The message of their study is that early CTO-PCI in patients with STEMI presenting with a concurrent CTO during primary PCI should not be performed routinely.
The authors also analysed the study population combined and found higher long-term mortality in patients who were older (>60 years) (11% vs 3%; HR 3.74; 95% CI 1.37 to 10.21; P=0.01), who had diabetes (15% vs 6%; HR 2.94; 95% CI 1.19 to 7.30; P=0.02), had a higher left ventricular enddiastolic volume at baseline (12% vs 1%; HR 13.04; 95% CI 1.70 to 100.30; P=0.01) and who had a high SYNTAX score (10% vs 4%; HR 2.50; 95% CI 1.01 to 6.20; P=0.048). They also stated that cardiac death was more frequent in the CTO-PCI arm (6.0% vs 1.0%, P=0.02) with no difference in all-cause mortality. However, it is known that a major prognostic factor in STEMI patients with a concurrent CTO is the presence of collateral feeding donor arteries from an infarct-related artery (IRA). Of patients with CTO, those with collateral flow from the IRA have significantly higher mortality than the non-IRA group (at 30 days: 52.2% vs. 10.9%, P<0.0001).[2] Obviously, in acute phase of these unstable conditions, the myocardium in the “remote” zone of infarction (CTO-zone) also ceases to contract. It is uncertain whether primary angioplasty in the IRA led to recover in the contractile function in the CTO zone. It would be very helpful if Elias et al could provide additional angiographic data regarding the IRA and the donor artery of CTO in their population (and the impact of PCI-CTO in this group). Surprisingly, in most post-myocardial infarction PCI-CTO studies relevant data are lacking.
1. Elias J, van Dongen IM, Råmunddal T, Laanmets P, et al. Long-term impact of chronic total occlusion recanalisation in patients with ST-elevation myocardial infarction. Heart. 2018 Feb 20. pii: heartjnl-2017-312698. doi: 10.1136/heartjnl-2017-312698. [Epub ahead of print]
2. Fujii T, Sakai K, Nakano M, et al. Impact of the origin of the collateral feeding donor artery on short-term mortality in ST-elevation myocardial infarction with comorbid chronic total occlusion. Int J Cardiol. 2016;218:158-163.
Dear Editor,
With great interest, I read the article by Sainsbury and associates[1] and congratulate them for extensively reviewing the unsolved issue of refractory angina. How many suffer from this condition worldwide remains unclear. However, it is believed that hundreds of thousands of Americans are affected, and that this number increases annually. Likely, millions are affected worldwide. Diffuse coronary artery disease is the main reason for refractory angina, because such arteries are non-amenable to percutaneous interventions or bypass grafting. Comorbidities are a second reason, especially in our aging population. Yet history is a cycle; medicine’s history no exception. Old concept, experiments, and theories that have fallen by the wayside can sometimes be resurrected and re-explored, released from the technological constraints of their time. The coronary sinus reducer system is one good example, since the concept stems from studies on the effects of cardiac vein ligation performed in the 1930s by Canadian surgeon Mercier Fauteux[2]. Two additional concepts might be resurrected and adapted to modern technologies. One is the concept of internal mammary artery (IMA) occlusion which, at that time, was performed through a small bilateral incision between the second and third ribs. The belief was that localized hypertension superior to the obstruction increased perfusion pressure in channels leading to the heart, specifically through the peri-cardio-phrenic br...
Dear Editor,
With great interest, I read the article by Sainsbury and associates[1] and congratulate them for extensively reviewing the unsolved issue of refractory angina. How many suffer from this condition worldwide remains unclear. However, it is believed that hundreds of thousands of Americans are affected, and that this number increases annually. Likely, millions are affected worldwide. Diffuse coronary artery disease is the main reason for refractory angina, because such arteries are non-amenable to percutaneous interventions or bypass grafting. Comorbidities are a second reason, especially in our aging population. Yet history is a cycle; medicine’s history no exception. Old concept, experiments, and theories that have fallen by the wayside can sometimes be resurrected and re-explored, released from the technological constraints of their time. The coronary sinus reducer system is one good example, since the concept stems from studies on the effects of cardiac vein ligation performed in the 1930s by Canadian surgeon Mercier Fauteux[2]. Two additional concepts might be resurrected and adapted to modern technologies. One is the concept of internal mammary artery (IMA) occlusion which, at that time, was performed through a small bilateral incision between the second and third ribs. The belief was that localized hypertension superior to the obstruction increased perfusion pressure in channels leading to the heart, specifically through the peri-cardio-phrenic branch[3]. Recently, I have resurrected this concept and suggested performing endovascular occlusion of the IMAs[4]. More recently, others have demonstrated that occluding the IMAs arteries could increase the collateral flow index and fractional flow reserve ipsilaterally, while decreasing angina[5]. These data are encouraging and spur further investigations. However, I also feel that Vineberg’s operation, consisting of tunnelization of IMAs into the left ventricle wall, is worthy of resurrection. This procedure, performed for about two decades, once was successful at relieving angina[2]. A huge collateral network developed between the IMAs and coronary arteries, and the IMAs often remained patent even at long-term follow-up. There is no reason to a-priori exclude IMA intra-myocardial tunnelization in patients for whom bypass is contraindicated, and vast opportunities exist for novel experimental and clinical studies on this technique.
Words = 345
References
1. Sainsbury PA, Fisher M, de Silva R. Alternative interventions for refractory angina. Heart. 2017 ;103(23):1911-1922.
2. Picichè M. The history of myocardial revascularization before the advent of cardiopulmonary bypass, in: M. Picichè (Ed.), Dawn and Evolution of Cardiac Procedures:Research Avenues in Cardiac Surgery and Interventional Cardiology, Springer- Verlag, Heidelberg 2012, pp. 65–77.
3. Picichè M. Noncoronary Collateral Myocardial Blood Flow: The Human Heart’s Forgotten Blood Supply. The Open Cardiovasc Med J 2015; 9:105-113.
4. Picichè M. Embolization of the internal thoracic arteries in refractory angina. Int J Cardiol. 2016;212:310.
5. Stoller M, Seiler C. Effect of permanent right internal mammary artery closure on coronary collateral function and myocardial ischemia. Circ Cardiovasc Interv 2017;10:e004990.
The recommendation that combined antiplatelet and new oral anticoagulant(NOAC) therapy should rely on the lowest approved NOAC dose effective for stroke prevention(1) is one which favours low-dose edoxaban instead of either dabigatran, rivaroxaban, or apixaban, when reduction of risk of gastrointestinal(GIT) bleeding is taken into account. In a review of clinical experience of bleeding associated with NOACs(dabigatran, rivaroxaban, apixaban, and edoxaban) versus warfarin in nonvalvular atrial fibrillation(NVAF), edoxaban 30 mg/day was the only antithrombotic agent associated with significantly(p < 0.001) lower risk of GIT bleeding than warfarin(Hazard Ratio: 0.67;95% Confidence Interval 0.53 to 0.83). For apixaban and for dabigatran 110 mg BID, the risk of GIT bleeding was comparable with the risk associated with warfarin use. For rivaroxaban and for dabigatran 150 mg BID the risk of GIT haemorrhage was significantly higher(P < 0.0001, and p < 0.001, respectively) than the GIT bleeding risk associated with warfarin(2).
Show MoreIn a study where 92.2% of 5301 NVAF users of antiplatelet agents were prescribed a NOAC in combination with only one antiplatelet agent vs 86.3% of 9106 NVAF users of antiplatelet agents who were prescribed warfarin with only one antiplatelet agent , concomitant antiplatelet and NOAC use was associated with significantly lower risk of intracranial bleeding than concomitant antiplatelet and warfarin use(HR 0.68, 95% CI, 0.51 to 0.91). Ne...
Given the fact that constrictive pericarditis is an eminently reversible cause of congestive heart failure(CHF) its timely clinical recognition deserved special mention in the recent review of epidemiology of pericardial diseases in Africa(1). Timely recognition and treatment might, arguably, mitigate the risk of perioperative mortality which is currently of the order of 12.5% to 14%, given the fact that this adverse statistic is principally generated by patients who come to operation in New York Heart Association functional class III and IV(2)(3). Accordingly, what needs to be done is to educate doctors and medical students to identify stigmata which differentiate CP from "run of the mill" CHF so as to expedite early referral of suspected CP to tertiary centres for definitive diagnosis and, hence, timely pericardiectomy.
Show MoreAccording to Little and Freeman, in the typical case of CP, "there will be marked jugular venous distension, hepatic congestion, ascites, and peripheral oedema, while the lungs remain clear"(3). Consequently, on the basis of their series of 30 patients, Evans and Jackson observed that "the presence of distended neck veins in a patient who is able to lie comfortably in the recumbent posture is characteristic of the disease"(4). The jugular venous pressure(JVP) response to a diagnostic trial of diuretic therapy may also be of diagnostic significance(5)(6). In CP, the typical response is that the JVP remains persisten...
We read with interest the article by Rusingiza et al (1)and report our experience from Northern Sri Lanka, a Low Middle Income Country (LMIC). Sri Lanka had invested heavily in free education and healthcare with demonstrably high literacy rates and positive health indices (2). However, the focus of the healthcare related investment has been in the secondary and tertiary care institutions, whilst primary care systems remain poorly developed. Northern Sri Lanka had been further impacted adversely by three decades of civil strife.
Show MoreWe report our experience in the management of post-valvular surgery patients at the Jaffna Teaching Hospital, the only tertiary referral centre for the region. Improvements in socioeconomic conditions has resulted in a decline in the incidence of rheumatic heart disease in Sri Lanka which accounted for only 0.34% of all deaths in 2017 (3). Concurrently, established patients receiving prosthetic heart valves has increased mainly due to improving access to surgical facilities. Unfortunately, Northern Sri Lanka had been without facilities for cardiac surgery for three decades leaving patients to access facilities elsewhere in the country. Post-surgery follow-up occurred primarily in Jaffna and a few other secondary care hospitals in the region. Unlike in the Rwandan study, most of our patients received parenteral penicillin prophylaxis thereby enhancing compliance and were fitted with metallic rather than bioprosthetic valves, thereby necessitat...
To the Editor, we read with great interest the article by Ntiloudi et al[1], describing hospitalization for heart failure (HF) as a powerful predictor of mortality among adults with pulmonary hypertension related to congenital heart disease (PH-ACHD). Although pulmonary arterial hypertension (PAH) targeted therapy has improved their survival, long-term complications such as HF hospitalization commonly occurred, and dismal prognosis with a mortality rate of 18.5% deeply broke our heart, thus requiring earlier diagnosis, risk stratification and therapeutic intervention.
Show MoreHospitalization for HF, a sign of clinical worsening, is associated with poor outcomes and generally used as one of composite endpoints in PAH[2], Ntiloudi et al stated nearly one-quarter of patients were hospitalized for HF, and they encountered a ninefold increased mortality risk compared to those not-hospitalized, since NYHA functional class III/IV raised a tenfold risk of death, its combination with HF hospitalization may better predict outcomes. A previous study[3] reported 29% patients with idiopathic and associated PAH were hospitalized for acute right heart failure at least once during a 39.1-month follow up, and those with hospitalizations had worse NYHA functional class, inferior right ventricle function, lower six minute walk test (6MWT) distance and worse outcomes defined by death/transplant (67% vs 33%). These two findings indicated a potential role of HF hospitalization for identifying...
There was significantly higher usage of both loop diuretics and aldosterone antagonist in the group with persistent hyponatraemia. Is it possible that one of the clinical manifestation of RV dysfunction, i.e peripheral oedema, led to an increased use of diuretic in this group and hence hyponatraemia as a complication of this treatment? Over diuresis in this scenario leads to activation of the RAAS which in turn worsens pulmonary hypertension and tricuspid regurgitation. The consequence of this is worsening peripheral oedema and the tendency to increase the diuretic dose.Hyponatraemia therefore may not be an independent predictor of outcome as stated.
We read with great interest the article by Elias et al (1) regarding the longer term clinical outcomes from the EXPLORE trial. The authors are to be congratulated for conducting this important study to address the optimal management of patients presenting with a concurrent CTO in a non-infarct related artery (non-IRA) during a STEMI. The results at 1 year are similar to those in the initial 4 month outcome (2), with no difference in the primary endpoints of cardiac MRI determined LVEF or LVEDV in either CTO-PCI and CTO-No PCI groups. At a median of 3.9 years, there was no difference in long term MACE, although an apparent increase in cardiovascular mortality (6% vs 1%, p=0.02).
Whilst this important study adds to the much needed literature on randomised studies related to PCI of CTOs, the results should be interpreted with caution. Firstly, large scale contemporaneous studies in CTO PCI have had procedural success rates in the region of 90% (3), whilst in EXPLORE (2) this rate was considerably lower, at 73% by core laboratory. This suggests either a more anatomically complex subset of patients, or else attempts by non-dedicated CTO PCI operators, both of which affect the interpretation of the intention to treat population.
Furthermore, the mortality data should be reviewed with care. At 12 months, there were 4 cardiovascular deaths (2.7%) in the CTO PCI group, with no deaths in the CTO-No PCI groups. These rates are significantly lower compared with other t...
Show MoreWe thank dr. Katsouras for his response to our long-term EXPLORE manuscript (1). We agree that in the ST-segment elevation (STEMI) population the presence of collaterals to the concurrent chronic total occlusion (CTO) is of prognostic relevance. We previously reported in 413 consecutive STEMI patients with a CTO that the presence of well-developed collaterals to the CTO compared to poorly developed collaterals was associated with improved outcome. We also assessed the influence of the collateral origin on survival, as collaterals coming distally from the culprit lesion are (partially) blocked during the acute phase of STEMI. In 16% of the patients the collaterals originated directly or distal from the culprit lesion and these patients had a lower survival compared to the patients in whom the collaterals were not blocked during STEMI (2).
In the EXPLORE trial patients with well-developed collaterals to the CTO had a significantly better left ventricular (LV) function at 4 months follow-up. Nonetheless, we did not find a significant treatment effect of CTO-PCI on global LV function nor on clinical outcome in patients with poorly developed nor with well-developed collaterals (3). On a regional level we found that the recovery of segmental wall thickening of the dysfunctional CTO myocardium was better in patients with well-developed collaterals. However, no significant interaction of collateral quality on the effect of CTO PCI was found (4). In EXPLORE there were 34 p...
Show MoreI read with great interest the paper by Elias et al regarding the mid-term and long-term clinical outcome of the Evaluating Xience and left ventricular function in Percutaneous Coronary Interventions on occlusiOns afteR ST elevation myocardial infarction (EXPLORE) trial. [1] The authors are to be congratulated for this detailed analysis evaluating the effect of chronic total occlusions – percutaneous coronary intervention (CTO-PCI) compared with CTO-No PCI on clinical outcome, left ventricular function and angina status in patients with ST elevation myocardial infarction (STEMI) with a concurrent CTO. The message of their study is that early CTO-PCI in patients with STEMI presenting with a concurrent CTO during primary PCI should not be performed routinely.
Show MoreThe authors also analysed the study population combined and found higher long-term mortality in patients who were older (>60 years) (11% vs 3%; HR 3.74; 95% CI 1.37 to 10.21; P=0.01), who had diabetes (15% vs 6%; HR 2.94; 95% CI 1.19 to 7.30; P=0.02), had a higher left ventricular enddiastolic volume at baseline (12% vs 1%; HR 13.04; 95% CI 1.70 to 100.30; P=0.01) and who had a high SYNTAX score (10% vs 4%; HR 2.50; 95% CI 1.01 to 6.20; P=0.048). They also stated that cardiac death was more frequent in the CTO-PCI arm (6.0% vs 1.0%, P=0.02) with no difference in all-cause mortality. However, it is known that a major prognostic factor in STEMI patients with a concurrent CTO is the presence of collateral feeding...
I read with interest the bright review of stable coronary syndromes (1). In the formation of the fetal muscular part
of the interventricular septum (IVS), the expanding ventricles grow and their medial walls approach and fuse, forming
the septum. The inside corner between the septum and the right anterior ventricular wall exhibits the deep pits being
called interventricular sinuses (ISs). The IS passes through the right IVS formed from the medial wall of the expanding
fetal right ventricle (RV). The opening of the interventricular vessel (IV) (kuuselian vessel) is located in the IS between
the medial walls of the expanding fetal RV and fetal left ventricle (LV). The IV is not a canal or channel or blood
vessel, but a slit between the fibres of the muscle to the outer layer of the left central muscular part of the IVS and runs
at an angle of about 90 degrees through sphincter and the left IVS into the LV. The IV exhibits 2 to 3 oval 2x5 mm
openings in the left central muscular part of the IVS surrounded by the interventricular sphincter (ISP). The ISP and the
IV are feasible to be patent by relaxing and widening of the helical heart at the right atrial filling phase at the end of the
fetal diastole. The left to right communication do not result as the earliest left ventricular activation close the ISP. The
sinoatrial node initially activates the right atrium (RA), followed by activation...
Show MoreDear Editor,
Show MoreWith great interest, I read the article by Sainsbury and associates[1] and congratulate them for extensively reviewing the unsolved issue of refractory angina. How many suffer from this condition worldwide remains unclear. However, it is believed that hundreds of thousands of Americans are affected, and that this number increases annually. Likely, millions are affected worldwide. Diffuse coronary artery disease is the main reason for refractory angina, because such arteries are non-amenable to percutaneous interventions or bypass grafting. Comorbidities are a second reason, especially in our aging population. Yet history is a cycle; medicine’s history no exception. Old concept, experiments, and theories that have fallen by the wayside can sometimes be resurrected and re-explored, released from the technological constraints of their time. The coronary sinus reducer system is one good example, since the concept stems from studies on the effects of cardiac vein ligation performed in the 1930s by Canadian surgeon Mercier Fauteux[2]. Two additional concepts might be resurrected and adapted to modern technologies. One is the concept of internal mammary artery (IMA) occlusion which, at that time, was performed through a small bilateral incision between the second and third ribs. The belief was that localized hypertension superior to the obstruction increased perfusion pressure in channels leading to the heart, specifically through the peri-cardio-phrenic br...
Pages