Low Transvalvular Flow Rate in Patients Undergoing Transcatheter Aortic Valve Implantation (TAVI) Is a Predictor of Mortality: The TFR-TAVI Study.

BACKGROUND: Transvalvular flow rate (TFR) represents a better reflection of transvalvular flow than the stroke volume index (SVi), and has recently emerged as a useful prognostic tool in patients undergoing surgical aortic valve replacement. There is a paucity of data investigating the role of TFR and its relationship with other clinical or echocardiographic factors in patients undergoing transcatheter aortic valve implantation (TAVI). METHOD: This was a retrospective single-centre study of 629 consecutive patients who underwent TAVI between March 2009 and September 2020. Pre-TAVI low TFR was defined as <200 c/s. The primary study end point was all-cause mortality. RESULTS: Low TFR was observed in 41.8% (263/629) of included patients and was associated with increasing age, low body surface area, hypertension, diabetes, atrial fibrillation, left ventricular (LV) dysfunction, and significant mitral regurgitation. LV function status and severity of aortic valve disease were independent predictors of low TFR. Low TFR was significantly associated with long-term all-cause mortality even after adjustment for other risk factors (adjusted hazard ratio [aHR] 1.44; 95% confidence interval [CI] 1.02-2.03; p=0.038). When data were stratified according to SVi, low TFR was an independent predictor of long-term all-cause mortality in patients with normal SVi (aHR 1.98; 95% CI 1.06-3.69; p=0.032) but not in patients with low SVi (HR 1.23; 95% CI 0.71-2.11; p=0.46; p=0.016 for interaction). CONCLUSIONS: Low TFR is common in patients undergoing TAVI and is an independent predictor of all-cause mortality, particularly in patients with normal SVi.

Coronary revascularization in patients with left ventricle systolic dysfunction, current challenges and clinical outcomes.

The effects of coronary revascularization in patients with left ventricle systolic dysfunction (LVSD) are not well studied. The decision about revascularization and its timing remain challenging, not only related to procedural risk, but also linked to other several limitations including assessment of ischemia, viability, and ability to predict LV recovery. The role of viability as a prognostic marker for patients with LVSD and its use as a therapeutic target remains debatable. In this article, we will review the role of LVSD in patients undergoing coronary revascularization alongside the role of ischemia and viability assessment. We will provide a review of the literature on the outcomes of coronary revascularization, both surgically and percutaneously, in patients with LVSD.

Mechanical circulatory support in acute myocardial infarction complicated by cardiogenic shock.

Patients with acute myocardial infarction (MI) complicated by cardiogenic shock (CS) have poor prognosis. Over the last two decades, there has been some improvement in mortality rates associated with CS. Initial measures to stabilise patients should follow a shock protocol, including therapies such as volume expansion, inotropes/vasopressors, and early coronary revascularisation. The use of mechanical circulatory support (MCS) devices demonstrated better haemodynamic and metabolic profiles for patients with CS. However, these benefits have not been consistently translated into significant reductions in cardiovascular adverse events. This review aims to discuss emerging concepts related to CS including an update on its classification and pathophysiology. The focus is on recent evidence regarding the use of MCS and the timing of initiating in patients with CS.

Clinical outcomes of percutaneous coronary intervention in high-risk patients turned down for surgical revascularization.

AIMS: There are limited data on outcomes of PCI in surgical turndown patientsespecially in those presenting with ACS. METHODS AND RESULTS: A retrospective analysis of prospectively collected data of patients who were turned down for CABG and had PCI between 2013 and 2020. All consecutive patients (449), ACS (n = 245) and no-ACS (n = 204) were included. In-hospital complications occurred in 28 patients (6.2%). At 30 days, 27 patients (6.0%) died (18 patients in the ACS group [7.3%] vs. 9 patients in the no-ACS group [4.4%], p = 0.23). Following multivariate analysis, no significant difference in long-term mortality was observed between the two groups (median follow-up of 4 [2-6] years, hazard ratio [HR]: 1.08, 95% confidence interval [CI]: 0.75-1.58, p = 0.667). In propensity score-matched analysis, the adjusted mortality risk was also not different between the groups (HR: 0.74, 95% CI: 0.25-1.26, p = 0.374). Independent predictors of mortality included chronic kidney disease stage ≥ 3 (HR: 1.64, 95% CI: 1.13-2.39, p = 0.009), high European System for Cardiac Operative Risk Evaluation II (HR: 1.02, 95% CI: 1.00-1.05, p = 0.035), and laser atherectomy use (HR: 3.35, 95% CI: 1.32-8.54, p = 0.011). CONCLUSIONS: PCI in surgical patients turndown patients appears safe. ACSpresentation was associated with more comorbid illnesses; however, afteradjustment, ACS did not independently confer additional risk of mortality.

Arginine Vasopressin Plays a Role in Microvascular Dysfunction After ST-Elevation Myocardial Infarction.

Background Coronary microvascular dysfunction (CMD) predicts mortality after ST-elevation-myocardial infarction (STEMI). Arginine vasopressin (AVP) may be implicated, but data in humans are lacking, and no study has investigated the link between arginine vasopressin and invasive measures of CMD. Methods and Results We invasively assessed CMD in 55 patients with STEMI treated with primary percutaneous coronary intervention (PPCI), by measuring the index of microcirculatory resistance after PPCI. In a separate group of 45 patients with STEMI/PPCI, recruited for a clinical trial, we measured infarct size and microvascular obstruction with cardiac magnetic resonance (CMR) imaging at 1 week and 12 weeks post-STEMI. Serum copeptin was measured at 4 time points before and after PPCI in all patients with STEMI. Plasma copeptin levels fell from 92.5 pmol/L before reperfusion to 6.4 pmol/L at 24 hours. Copeptin inversely correlated with diastolic, but not systolic, blood pressure (r=-0.431, P=0.001), suggesting it is released in response to myocardial ischemia. Persistently raised copeptin at 24 hours was correlated with higher index of microcirculatory resistance (r=0.372, P=0.011). Patients with microvascular obstruction on early CMR imaging showed a trend toward higher admission copeptin, which was not statistically significant. Copeptin levels were not associated with infarct size on either early or late CMR. Conclusions Patients with CMD after STEMI have persistently elevated copeptin at 24 hours, suggesting arginine vasopressin may contribute to microvascular dysfunction. Arginine vasopressin receptor antagonists may represent a novel therapeutic option in patients with STEMI and CMD.

Meta-analysis Comparing Long-Term Clinical Outcomes of Percutaneous Coronary Intervention versus no Intervention in Patients with Chronic Total Occlusion.

Chronic total occlusion (CTO) percutaneous coronary intervention (PCI) has substantially improved due to increasing operator experience and advancements in equipment, techniques, and management algorithms. However, the overall benefit of CTO PCI remains controversial, particularly since only a few randomized trials have been reported to date. Methods: We performed a meta-analysis to evaluate the efficacy of CTO PCI. The study outcomes were the occurrence of all-cause mortality, myocardial infarction, repeat revascularization, stroke, or freedom from angina at the longest documented follow-up period. Results: In five trials including 1790 patients, the mean age was 63 ± 10 years, 17% were female, with a median follow-up of 2.9 years. The procedural success rate ranged from 73% to 97% and the right coronary artery was the most involved artery (52%). There was no significant difference between CTO PCI and no intervention regarding all-cause mortality (odds ratio [OR]: 1.10, 95% confidence interval [CI]: 0.49-2.47, P = 0.82), myocardial infarction (OR: 1.20, 95% CI: 0.81-1.77, P = 0.36), repeat revascularization (OR: 0.67, 95% CI: 0.40-1.14, P = 0.14), or stroke (OR: 0.60, 95% CI: 0.26-1.36, P = 0.22). In two trials including 686 patients, significantly more patients were free of angina at 1 year, defined as the Canadian Cardiovascular Society grading of angina pectoris Grade 0, in the CTO PCI group compared to the no intervention group (OR: 0.52, 95% CI: 0.35-0.76, P < 0.001). Meta-regression analyses based on various trial-level covariates (gender, diabetes, previous myocardial infarction, PCI or coronary artery bypass graft, SYNTAX or J-CTO scores, and CTO-related artery percentages) did not suggest any statistically significant relationships. Conclusions: CTO PCI appears to have a similar efficacy profile compared to no intervention at long-term follow-up, but with a significant improvement of angina favoring PCI-treated patients. Further adequately powered and long-term trials are required to identify the best management strategy for patients with coronary CTO.

Magnetic Resonance Left Ventricle Mass-Index/Fibrosis: Long-Term Predictors for Ventricular Arrhythmia in Hypertrophic Cardiomyopathy-A Retrospective Registry.

Objective: We aimed to study the long-term association of LV mass index (LVMI) and myocardial fibrosis with ventricular arrhythmia (VA) in a population of patients with confirmed hypertrophic cardiomyopathy (HCM) using cardiac magnetic resonance imaging (CMR). Methods: We retrospectively analyzed the data in consecutive HCM patients confirmed on CMR referred to an HCM clinic between January 2008 and October 2018. Patients were followed up yearly following diagnosis. Baseline demographics, risk factors and clinical outcomes from cardiac monitoring and an implanted cardioverter defibrillator (ICD) were analyzed for association of LVMI and LV late gadolinium enhancement (LVLGE) with VA. Patients were then allocated to one of two groups according to the presence of VA (Group A) or absence of VA (Group B) during the follow-up period. The transthoracic echocardiogram (TTE) and CMR parameters were compared between the two groups. Results: A total of 247 patients with confirmed HCM (age 56.2 ± 16.6, male = 71%) were studied over the follow-up period of 7 ± 3.3 years (95% CI = 6.6-7.4 years). LVMI derived from CMR was higher in Group A (91.1 ± 28.1 g/m2 vs. 78.8 ± 28.3 g/m2, p = 0.003) when compared to Group B. LVLGE was higher in Group A (7.3 ± 6.3% vs. 4.7 ± 4.3%, p = 0.001) when compared to Group B. Multivariable Cox regression analysis showed LVMI (hazard ratio (HR) = 1.02, 95% CI = 1.001-1.03, p = 0.03) and LVLGE (HR = 1.04, 95% CI = 1.001-1.08, p = 0.04) to be independent predictors for VA. Receiver operative curves showed higher LVMI and LVLGE with a cut-off of 85 g/m2 and 6%, respectively, to be associated with VA. Conclusions: LVMI and LVLGE are strongly associated with VA over long-term follow-up. LVMI requires more thorough studies to consider it as a risk stratification tool in patients with HCM.

Colchicine for the prevention of ischemic stroke: An updated meta-analysis of randomized clinical trials.

BACKGROUND: Inflammation is increasingly recognized as a target to reduce residual cardiovascular risk. Colchicine is an anti-inflammatory drug that was associated with improved cardiovascular outcomes. However, its effect on stroke reduction was not consistent across studies. Therefore, the aim of this study-level meta-analysis was to evaluate the influence of colchicine on stroke in patients with coronary artery disease (CAD). METHODS: Electronic databases were searched through October 2020, to identify randomized controlled trials using colchicine in patients with CAD. The incidence of clinical endpoints such as stroke, death, myocardial infarction (MI), study-defined major adverse cardiovascular events (MACE), and atrial fibrillation (AF) was compared between colchicine and placebo groups. RESULTS: A total number of 11,594 (5,806 in the colchicine arm) patients from 4 eligible studies were included in the final analysis. Stroke incidence was lower in the colchicine arm compared to placebo (rate ratio [RR] 0.48 [95% confidence interval [CI], 0.29-0.78], P = 0.003) whereby no significant difference was observed in the incidence of AF (odds ratio [OR] 0.86 [95% CI, 0.69-1.06], P = 0.16). Furthermore, a significant effect of colchicine on MACE [RR 0.65 (95% CI, 0.51-0.83), P = 0.0006] and MI (RR 0.65 (95% CI, 0.54-0.95], P = 0.02) was detected, with no influence on all-cause mortality (RR 1.04 [95% CI, 0.61-1.78], P = 0.88). CONCLUSIONS: This meta-analysis confirms a significant influence of colchicine on stroke in CAD patients. Despite its neutral effect on AF occurrence, other mechanisms related to plaque stabilization are plausible. The concept seems to be supported by contemporaneous MI reduction and posits that anti-inflammatory properties of colchicine may translate into a reduction of stroke risk.

Intensive lipid-lowering therapy, time to think beyond low-density lipoprotein cholesterol.

Statins have been shown to be effective in reducing cardiovascular events. Their magnitude of benefits has been proportionate to the reduction in low-density lipoprotein cholesterol (LDL-c). Intensive lipid-lowering therapies using ezetimibe and more recently proprotein convertase subtilisin kexin 9 inhibitors have further improved clinical outcomes. Unselective application of these treatments is undesirable and unaffordable and, therefore, has been guided by LDL-c level. Nonetheless, the residual risk in the post-statin era is markedly heterogeneous, including thrombosis and inflammation risks. Moreover, the lipo-protein related risk is increasingly recognised to be related to other non-LDL-c markers such as Lp(a). Emerging data show that intensive lipid-lowering therapy produce larger absolute risk reduction in patients with polyvascular disease, post coronary artery bypass graft and diabetes. Notably, these clinical entities share similar phenotype of large burden of atherosclerotic plaques. Novel plaque imaging may aid decision making by identifying patients with propensity to develop lipid rich plagues at multi-vascular sites. Those patients may be suitable candidates for intensive lipid lowering treatment.

Accessory Mitral Valve Tissue Causing Features Of Left Ventricular Outflow Tract Obstruction-A Case Report And Updated Literature Review.

Accessory mitral valve tissue is a rare congenital anomaly that is commonly incidentally diagnosed. When symptomatic, it tends to present with features of left ventricular outflow (LVOT) obstruction in about two thirds of cases. It is also commonly associated with other congenital anomalies, notably ventricular septal defects. Transthoracic echocardiography is a very useful diagnostic test to make a diagnosis and its widespread use will increase detection of this condition. We are presenting a case of a 29-year-old lady who presented with breathlessness in the third trimester of pregnancy and was subsequently found to have evidence of accessory mitral valve tissue on echocardiography.

The safety and effectiveness of statins as treatment for HIV-dyslipidemia: the evidence so far and the future challenges.

INTRODUCTION: Statin therapy is widely used across the globe for the treatment and prevention of cardiovascular disease (CVD). It is well established that statin therapy is associated with significant decrease in low-density lipoprotein cholesterol (LDL-C) and plasma cholesterol levels. HIV-dyslipidemia is a common problem with extensive use of combination antiretroviral therapy (CART), and is associated with an increase in incidence of cardiovascular disease (CVD), resulting in hospital admission and surgery throughout the western healthcare systems. AREAS COVERED: This review describes the effectiveness and safety of statins in the treatment of HIV-dyslipidemia. Medline was searched for different statins as treatment for HIV-dyslipidemia. EXPERT OPINION: Dyslipidemia in patients with HIV is different from the normal population, due to the fact that HIV treatment may not only cause dyslipidemia, but may also interact with lipid lowering medication. Statin-unresponsive HIV-dyslipidemia can be treated with the addition of ezetimibe, fenofibrate, fish oil and niacin. Current guidelines recommend the use of pravastatin and atorvastatin as first-line therapy, whereas European guidelines include rosuvastatin. There is an urgent need to confirm whether the use of statins in HIV-dyslipidemia is associated with an increase in the incidence of diabetes; this is significant because HIV patients are known to be insulin-resistant. HIV is also associated with Non-alcoholic Fatty Liver Disease (NAFLD), a condition known to be associated with insulin resistance. Further clinical trials are urgently needed to assess the impact of statins on CVD in HIV patients, and future challenges for researchers in this area are enormous.