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Background Functional mitral regurgitation (FMR) has emerged as a therapeutic target in patients with chronic heart failure and left ventricular systolic dysfunction. The significance of FMR in acute decompensated heart failure remains obscure. We systematically investigated the prevalence and clinical significance of FMR on admission in patients admitted with acute decompensated heart failure and left ventricular systolic dysfunction. Methods and Results The study was a single‐center, retrospective review of patients admitted with acute decompensated heart failure and left ventricular systolic dysfunction between 2012 and 2017. Patients were divided into 3 groups of FMR: none/mild, moderate, and moderate‐to‐severe/severe FMR. The primary outcome was 1‐year post‐discharge all‐cause mortality. We also compared these groups for 6‐month heart failure hospitalization rates. Of 2303 patients, 39% (896) were women. Median left ventricular ejection fraction was 25%. Four hundred and fifty‐three (20%) patients had moderate‐to‐severe/severe FMR, which was independently associated with 1‐year all‐cause mortality. Moderate or worse FMR was found in 1210 (53%) patients and was independently associated with 6‐month heart failure hospitalization. Female sex was independently associated with higher severity of FMR. Conclusions More than half of patients hospitalized with acute decompensated heart failure and left ventricular systolic dysfunction had at least moderate FMR, which was associated with increased readmission rates and mortality. Intensified post‐discharge follow‐up should be undertaken to eliminate FMR amenable to pharmacological therapy and enable timely and appropriate intervention for persistent FMR. Further studies are needed to examine sex‐related disparities in FMR.

Introduction: Left ventricular (LV) global longitudinal strain (GLS) is a robust LV systolic function measure used to detect subtle chemotherapy cardiotoxicity. However, inter-reader and inter-vendor variabilities compromise the clinical value of longitudinal follow-up of GLS. Artificial intelligence (AI)-based, fully automated measurement of longitudinal strain may be more reliable compared with human interpretation. Methods: We studied 52 transthoracic echocardiographic examinations randomly selected from a Cardio-oncology registry. All subjects received anthracycline-based chemotherapy in 2016-2019. AI-based longitudinal strain was assessed by EchoGo Core using standard 2- and 4-chamber apical views. Two readers verified the myocardium tracing by AI and found no errors. Longitudinal strain results by EchoGo were compared to GLS measured by conventional software (TomTec and Philips QLAB) using standard 3-, 2- and 4-chamber apical views. Results: AI-based longitudinal strain analysis was feasible in 51/52 (98%) transthoracic echocardiographic studies. The mean longitudinal strain was -17.3±3.3% for EchoGo, -16.9±2.4% for TomTec and -17.5±3.1% for QLAB. Bland-Altman analysis showed a bias of -0.4 ± 2.7% and 95% limits of -5.7 to 4.9% between EchoGo longitudinal strain and TomTec GLS (Figure 1A). A bias of 0.2 ± 3.3% and 95% limits of -6.2 to 6.6% between EchoGo longitudinal strain and QLAB GLS (Figure 1B) were seen. The bias between TomTec GLS and QLAB GLS was 0.6 ±2.2% (Figure 1C). The inter-reader correlation coefficients of TomTec GLS and QLAB GLS were 0.57 and 0.71, respectively. Conclusions: This novel AI-based longitudinal strain analysis was feasible in the majority of echocardiograms without any operator input. The bias between EchoGo longitudinal strain and conventional software appears small. AI-based myocardial strain analysis may reduce variabilities and facilitate longitudinal follow-up of GLS in Cardio-oncology patients.

BACKGROUND HIV and HCV have each been linked with cardiac dysfunction. Studies of HIV have often lacked appropriate controls and primarily involved men, whereas data for HCV are sparse. METHODS We performed repeat echocardiography over a median interval of 12 years in participants from the Women's Interagency HIV Study in order to evaluate the relationships of HIV and HCV with incident left ventricular (LV) dysfunction (systolic or diastolic). RESULTS Of the 311 women included (age 39 ± 9), 70% were HIV-positive and 20% HCV-positive. Forty three participants (13.8%) developed LV dysfunction, of which 79.1% was diastolic. Compared with participants with neither infection, the group with HIV--HCV coinfection showed a significantly increased risk of incident LV dysfunction after adjustment for risk factors [RR = 2.96 (95% CI = 1.05-8.31)], but associations for the HCV monoinfected and HIV monoinfected groups were not statistically significant [RR = 2.54 (0.83-7.73) and RR = 1.66 (0.65-4.25), respectively]. Comparison of HCV-positive and HCV-negative women showed a significantly increased risk independent of covariates [RR = 1.96 (1.02-3.77)] but this was not the case for HIV-positive vs. HIV-negative women [RR = 1.43 (0.76-2.69)]. There was no evidence of HCV-by-HIV interaction. A more restrictive definition of LV diastolic dysfunction led to fewer incident cases, but a similar, though nonsignificant, risk estimate for HCV. CONCLUSION Among mostly middle-aged women, HCV but not HIV infection was associated with a pronounced risk of incident LV dysfunction. Although the influence of residual confounding cannot be excluded, these findings bolster the potential benefits that could be realized by adopting recent recommendations for expanding HCV screening and treatment.

Background Severe coronavirus disease 2019 (COVID‐19) is characterized by a proinflammatory state with high mortality. Statins have anti‐inflammatory effects and may attenuate the severity of COVID‐19. Methods and Results An observational study of all consecutive adult patients with COVID‐19 admitted to a single center located in Bronx, New York, was conducted from March 1, 2020, to May 2, 2020. Patients were grouped as those who did and those who did not receive a statin, and in‐hospital mortality was compared by competing events regression. In addition, propensity score matching and inverse probability treatment weighting were used in survival models to examine the association between statin use and death during hospitalization. A total of 4252 patients were admitted with COVID‐19. Diabetes mellitus modified the association between statin use and in‐hospital mortality. Patients with diabetes mellitus on a statin (n=983) were older (69±11 versus 67±14 years; P P P P =0.82). Propensity score matching (hazard ratio, 0.88; 95% CI, 0.83–0.94; P P Conclusions Statin use was associated with reduced in‐hospital mortality from COVID‐19 in patients with diabetes mellitus. These findings, if validated, may further reemphasize administration of statins to patients with diabetes mellitus during the COVID‐19 era.

Introduction: The New York Governor Andrew M. Cuomo’s executive order N202.25 on March 7, 2020, canceled all elective, semi-urgent procedures, including cardiovascular interventions such as coronary angiography and angioplasty due to SARS- Cov2 (COVID 19) pandemic. New York City was devastated by COVID 19 infection carrying the highest incidence, prevalence, and mortality rates in the US. Importantly, a 4. 4.83-fold increase in death rate at home was reported. We hypothesized that the COVID19 surge postponed the patient's decision to seek medical attention leading to an increase in cardiovascular-related hospital mortality. Methods: We conducted a retrospective observational study examining the incidence, prevalence, complication rate, and mortality from cardiovascular diseases in hospitalized patients during COVID 19 surge. We performed a patient chart review of a cohort with acute cardiovascular events (STEMI, NSTEMI, Stroke, CHF) during the COVID 19 surge who were hospitalized at Montefiore Medical Center between March 7, 2020, and April 21, 2020, and compared it to a similar cohort from the preceding year (March 7, 2019 and April 21, 2019). Results: During the dates (March 7- April 21, 2020), there was a significant decrease in NSTEMI, stroke, and CHF admissions (P Conclusions: Montefiore Medical Center admitted and treated significantly fewer patients with acute cardiovascular syndromes during the COVID19 surge. Non-COVID patients presented with delayed MI. All HF patients (COVID+Non-COVID) carried a significantly higher mortality rate.

Introduction: Recent evidence suggests that complete revascularization (CR) of stable patients presenting with STEMI improves outcomes, but the appropriate timing of said CR has not been clearly established (CR during index PCI [iCR] versus staged CR [sCR]). sCR is defined as CR within a mean of 31.5±24.6 days after the STEMI. Objective: To determine the appropriate timing of CR for it to be beneficial (iCR versus sCR). Methods: A systematic review of Medline, Cochrane, and Embase was performed for randomized control trials (RCTs) that reported outcomes of stable patients presenting with STEMI and whose culprit lesion received PCI, who were subsequently randomized into culprit-lesion only and CR cohorts. Only RCTs with at least a 12-month follow-up were included. The timing of CR, for the subdivision of CR cohort into iCR and sCR, had to be stated. Seven RCTs comprising 6647 patients (mean age: 62.9±1.4 years, male sex: 79.4%) met this criteria and were included. Results: After a mean follow-up of 25.1±9.4 months, iCR, when compared to a culprit-lesion only strategy, was associated with a significant cardiovascular mortality benefit (Risk Ratio [RR] 0.48 95% Confidence Interval [CI] 0.26-0.90 p=0.02, Relative Risk Reduction [RRR] 52%) and a significant decrease in reinfarctions (RR 0.42 95% CI 0.25-0.70 p=0.001 RRR: 58%). sCR showed no significant benefit for any of the studied outcomes when compared to a culprit-lesion only strategy. There was no significant difference in all-cause mortality or in the composite safety outcome of contrast-induced nephropathy nor stroke in either the iCR or the sCR groups when compared to the culprit-lesion only group. Conclusion: Complete revascularization during index PCI of stable patients presenting with STEMI, but not staged CR, is associated with a statistically significant decrease in cardiovascular death and non-fatal reinfarctions. There is no difference between groups in all-cause mortality or in the composite safety outcome.

Background: The relationship between alcohol consumption and clinical heart failure has been extensively studied. There have been little longitudinal data documenting alcohol effects on cardiac structure and function in a community-based population. Methods: The second Echocardiographic Study of Latinos (ECHO-SOL2) was designed to provide echocardiographic parameters that characterized longitudinal cardiac structure and function in a random and representative sample of 1,818 participants ≥45 years old. Participants underwent to serial echocardiograms at 2011-2014 (exam 1) and ~5-6 years later at 2016-2019 (exam 2). Quantification of alcohol was created on a gender-specific basis. Multiple linear regression models were adjusted for age and sex. Results: The mean age at enrollment was 56.4 years old, 57% were women. At baseline, impaired left ventricular (LV) systolic function and increased right ventricular (RV) function were associated with binge drinkers (P = 0.01). At 5-6 years later, heavy drinkers had a significant decrease in LV ejection fraction (P = 0.01). Moderate and binge drinkers demonstrated worsening diastolic function over time (P ≤ 0.01). Binge drinkers demonstrated a progressive decrease in LV mass index (P = 0.02), decrease in LV stroke volume (P = 0.01) and further reduction in RV function (P < 0.01). Conclusion: Alcohol consumption was associated with longitudinal changes in cardiac structure and function, mostly among binge drinkers, which can lead to impaired myocardial contractility compared to nondrinkers.

A substantial proportion of patients with acute myocardial infarction develop clinical heart failure, which remains a common and major healthcare burden. It has been shown that in patients with chronic coronary artery disease, ischemic episodes lead to a global pattern of cardiomyocyte remodeling and dedifferentiation, hallmarked by myolysis, glycogen accumulation, and alteration of structural proteins. These changes, in conjunction with an impaired global coronary reserve, may eventually become irreversible and result in ischemic cardiomyopathy. Moreover, noninvasive imaging of myocardial scar and hibernation can inform the risk of sudden cardiac death. Therefore, it would be intuitive that imaging of myocardial viability is an essential tool for the proper use of invasive treatment strategies and patient prognostication. However, this notion has been challenged by large-scale clinical trials demonstrating that, in the modern era of improved guideline-directed medical therapies, imaging of myocardial viability failed to deliver effective guidance of coronary bypass surgery to a reduction of adverse cardiac outcomes. In addition, current available imaging technologies in this regard are numerous, and they target diverse surrogates of structural or tissue substrates of myocardial viability. In this document, we examine these issues in the current clinical context, collect current evidence of imaging technology by modality, and inform future directions.

Objective We carried out a meta-analysis summarizing the efficacy and safety of direct factor Xa inhibitor (DXI) in patients receiving guideline-based antiplatelet therapy (GBAT) after an acute coronary syndrome. Background Randomized-controlled trials have shown that the addition of a DXI to GBAT after acute coronary syndrome can reduce ischemic events, the trade-off being an increase in major bleeding complications. Methods PubMed, Central, Embase, The Cochrane Register, Google Scholar databases, and the scientific session abstracts were searched for eligible randomized trials from 1 January 1990 through 31 December 2016. Results Nine randomized-controlled trials were included in this meta-analysis enrolling a total of 45651 patients. There was a significant reduction in major adverse cardiovascular events with DXIs/GBAT compared with GBAT alone [odds ratio (OR): 0.88; 95% confidence interval (CI): 0.82-0.94, number needed to treat=52]. There were also significant reductions in two individual components of major adverse cardiovascular events: myocardial infarction (OR: 0.89; 95% CI: 0.81-0.98) and stent thrombosis (OR: 0.73; 95% CI: 0.59-0.90), favoring the DXI/GBAT group. There was an increased risk of major bleeding (OR: 2.51; 95% CI: 1.82-3.46) and intracranial hemorrhage (OR: 3.47; 95% CI: 1.76-6.86) compared with GBAT. Conclusion In acute coronary syndromes, the addition of a DXI to GBAT results in a significant reduction of major adverse cardiovascular events, myocardial infarction, and stent thrombosis, offset by an increased risk of bleeding.

James A. Arrighi, MD, FACC, Chair Lisa A. Mendes, MD, FACC, Co-Chair Jesse E. Adams III, MD, FACC John E. Brush Jr, MD, FACC[#][1] G. William Dec Jr, MD, FACC Ali Denktas, MD, FACC Susan Fernandes, LPD, PA-C Rosario Freeman, MD, MS, FACC[#][1] Rebecca T. Hahn, MD, FACC Jonathan L.

Background— A significant proportion of patients requiring aortic valve replacement (AVR) have undergone prior coronary artery bypass grafting (CABG). Reoperative heart surgery is associated with increased risk. Data on relative utilization and comparative outcomes of transcatheter (TAVR) versus surgical AVR (SAVR) in patients with prior CABG are limited. Methods and Results— We queried the 2012 to 2014 National Inpatient Sample databases to identify isolated AVR hospitalizations in adults with prior CABG. In-hospital outcomes of TAVR versus SAVR were compared using propensity-matched analysis. Of 147 395 AVRs, 15 055 (10.2%) were in patients with prior CABG. The number of TAVRs in patients with prior CABG increased from 1615 in 2012 to 4400 in 2014, whereas the number of SAVRs decreased from 2285 to 1895 ( P trend P =0.71) but lower incidence of myocardial infarction (1.5% versus 3.4%; P P P P Conclusions— TAVR is being increasingly used as the preferred modality of AVR in patients with prior CABG. Compared with SAVR, TAVR is associated with similar in-hospital mortality but lower rates of in-hospital complications in this important subset of patients.

Background: Metabolomics has provided new insights into mechanistic knowledge of CVD. However, this approach has limited use for studying arterial disease in high-risk women with and without HIV infection. Methods: Using liquid chromatography-tandem mass spectrometry, we profiled plasma levels of 114 cationic polar and 211 nonpolar lipid metabolites among 411 women (72% HIV+; 60% Black and 31% Hispanic) aged 35-50 from the Women’s Interagency HIV Study. Carotid arterial distensibility, a direct measure of carotid stiffness, was calculated from ultrasound measurements of the right common carotid artery diameter at systole and diastole and brachial artery pulse pressure measured. We performed partial least squares discriminant analysis (PLS-DA) to identify metabolite clusters associated with carotid stiffness (lowest vs. the other 3 quartiles of distensibility index). We used multivariate linear regression models to examine associations of individual metabolites with the distensibility index. Results: PLS-DA identified two major metabolite clusters associated with carotid stiffness. In the lipid metabolite cluster, triacylglycerols (TAGs 52:3, 52:4, 54:4), diacylglycerols (DAGs 36:2, 36:3) and sphingomyelins (16:1, 18:1, 18:2) were associated with decreased distensibility, while lysophosphatidylcholines (18:2, 20:5) were associated with increased distensibility. In the cationic polar metabolite cluster, urate, C4-OH carnitine, C5-DC carnitine, pseudouridine and 1-methyladenosine were associated with decreased distensibility. The associations of TAGs 52:3, 52:4, 54:4 and DAG 36:3 with carotid stiffness remained significant after further adjustment for conventional CVD risk factors ( Table ). No interaction by HIV infection was found. Conclusions: Among women with or at risk of HIV infection from predominantly race-ethnic minority groups, plasma TAGs and DAG of higher carbon number and double bond content are associated with carotid stiffness independent of conventional CVD risk factors.

Background— Prior studies have reported higher inhospital mortality in women versus men with non–ST-segment–elevation myocardial infarction. Whether this is because of worse baseline risk profile compared with men or sex-based disparities in treatment is not completely understood. Methods and Results— We queried the 2003 to 2014 National Inpatient Sample databases to identify all hospitalizations in patients aged ≥18 years with the principal diagnosis of non–ST-segment–elevation myocardial infarction. Complex samples multivariable logistic regression models were used to examine sex differences in use of an early invasive strategy and inhospital mortality. Of 4 765 739 patients with non–ST-segment–elevation myocardial infarction, 2 026 285 (42.5%) were women. Women were on average 6 years older than men and had a higher comorbidity burden. Women were less likely to be treated with an early invasive strategy (29.4% versus 39.2%; adjusted odds ratio, 0.92; 95% confidence interval, 0.91–0.94). Women had higher crude inhospital mortality than men (4.7% versus 3.9%; unadjusted odds ratio, 1.22; 95% confidence interval, 1.20–1.25). After adjustment for age (adjusted odds ratio, 0.96; 95% confidence interval, 0.94–0.98) and additionally for comorbidities, other demographics, and hospital characteristics, women had 10% lower odds of inhospital mortality (adjusted odds ratio, 0.90; 95% confidence interval, 0.89–0.92). Further adjustment for differences in the use of an early invasive strategy did not change the association between female sex and lower risk-adjusted inhospital mortality. Conclusions— Although women were less likely to be treated with an early invasive strategy compared with men, the lower use of an early invasive strategy was not responsible for the higher crude inhospital mortality in women, which could be entirely explained by older age and higher comorbidity burden.

Background— Nonvalvular atrial fibrillation is the most common arrhythmia. Patients with nonvalvular atrial fibrillation are at increased risk of stroke; therefore, we evaluated the efficacy and safety of different approaches to prevent this major complication. Methods and Results— We conducted electronic database searches of phase III randomized controlled trials. The groups were novel oral anticoagulants, Watchman left atrial appendage occlusion device (DEVICE), and warfarin. Efficacy outcomes were stroke or systemic embolism, and all-cause mortality. Safety outcome was major bleeding and procedure-related complications. A subgroup analysis of the elderly population was done. We used random-effects model to compare pooled outcomes and tested for heterogeneity. Odds ratios (ORs) and 95% confidence intervals (CIs) were computed for each outcome. Seven randomized controlled trials (n=73 978) were included. There was a significant difference favoring novel oral anticoagulants for systemic embolism (OR, 0.84; 95% CI, 0.72–0.97; P =0.01), all-cause mortality (OR, 0.89; 95% CI, 0.84–0.94; P P =0.026) compared with warfarin. No difference was seen between DEVICE and warfarin for efficacy end points; however, DEVICE had more complications (OR, 1.85; 95% CI, 1.14–3.01; P =0.012). In the elderly (6 randomized controlled trials, n=30 699), systemic embolism was favored with novel oral anticoagulants over warfarin (OR, 0.77; 95% CI, 0.68–0.87; P ≤0.001). No evidence of significant publication bias was found. Conclusions— Novel oral anticoagulants is superior to warfarin for stroke prevention in nonvalvular atrial fibrillation. This benefit was also observed in the elderly population. DEVICE is a reasonable noninferior alternative to warfarin for stroke prevention, but cautious use is essential given safety concerns.

Established coronary artery disease has a prevalence of 7% in adult Americans, accounting for 16 million people. As morbidity and mortality rates have risen, research efforts to identify the pathophysiologic mechanisms of systolic dysfunction have risen in parallel. The current goal is to develop new therapeutic strategies with the potential to reverse systolic dysfunction in patients with established coronary artery disease. Cardiac magnetic resonance imaging has gained a key role in cardio vascular medicine. We will comment on the potential pivotal role of cardiac magnetic resonance imaging for the assessment of myocardial viability, including hibernating and stunned myocardium and microvascular obstruction.

Imaging has become an indispensable tool in cardiovascular research, clinical trials, and medical practice. Traditional imaging modalities provide primarily anatomic as well as some physiological information. The emerging field of molecular imaging aims to expand beyond these traditional targets to visualize specific biochemical structures or biological processes. Platforms under exploration for molecular imaging include ultrasound, single-photon emission computed tomography (SPECT), positron emission tomography (PET), computed tomography (CT), magnetic resonance imaging (MRI), and optical techniques, such as fluorescence-mediated tomography (FMT) and catheter-based sensors. Ultimately, molecular imaging may allow clinicians to reach beyond anatomy to visualize the expression and activity of particular molecules, cells, or functions that influence disease progression, outcome, and/or responsiveness to therapeutics. The last 3 decades have seen explosive growth in the application of cardiovascular molecular imaging, as demonstrated by a recent PubMed search (Figure). Despite basic science advances, translation into clinically available agents and techniques has lagged. In September 2009 the National Heart, Lung, and Blood Institute (NHLBI) convened a working group of experts in the fields of molecular imaging and cardiovascular disease to assess the current state of molecular imaging and its application to cardiovascular diseases, to identify areas where cardiovascular molecular imaging was likely to have an impact, to explore barriers to the translation of molecular imaging toward clinical application, and to inform the NHLBI on national priorities for the promotion of translation of cardiovascular molecular imaging. Here, we summarize state-of-the-art technologies, their challenges, clinical needs, and specific recommendations of the working group. Figure. Cardiovascular molecular imaging publications from 1987 to 2010. The Scopus database was searched for the terms “molecular” and “imaging” in the title or abstract, and the results obtained were then restricted further by searching on “cardiovascular.” The results obtained from the restricted search were then checked manually to include only original research articles …

Background— Congestive heart failure in the setting of a preserved left ventricular (LV) ejection fraction is increasing in prevalence among the senior population. The underlying pathophysiologic abnormalities in ventricular function and structure remain unclear for this disorder. We hypothesized that patients with heart failure with preserved ejection fraction (HFPEF) would have marked abnormalities in LV diastolic function with increased static diastolic stiffness and slowed myocardial relaxation compared with age-matched healthy controls. Methods and Results— Eleven highly screened patients (4 men, 7 women) aged 73±7 years with HFPEF were recruited to participate in this study. Thirteen sedentary healthy controls (7 men, 6 women) aged 70±4 years also were recruited. All subjects underwent pulmonary artery catheterization with measurement of cardiac output, end-diastolic volumes, and pulmonary capillary wedge pressures at baseline; cardiac unloading (lower-body negative pressure or upright tilt); and cardiac loading (rapid saline infusion). The data were used to define the Frank-Starling and LV end-diastolic pressure-volume relationships. Doppler echocardiographic data (tissue Doppler velocities, isovolumic relaxation time, propagation velocity of early mitral inflow , E/A-wave ratio) were obtained at each level of cardiac preload. Compared with healthy controls, patients with HFPEF had similar LV contractile function and static LV compliance but reduced LV chamber distensibility with elevated filling pressures and slower myocardial relaxation as assessed by tissue Doppler imaging. Conclusions— In this small, highly screened patient population with hemodynamically confirmed HFPEF, increased end-diastolic static ventricular stiffness relative to age-matched controls was not a universal finding. Nevertheless, patients with HFPEF, even when well compensated, had elevated filling pressures, reduced distensibility, and increased diastolic wall stress compared with controls. In contrast, LV relaxation as assessed by tissue Doppler variables appeared consistently impaired in patients with HFPEF.

An asymptomatic 54-year-old man with severe mitral regurgitation caused by prolapse and pulmonary hypertension was referred for mitral valve surgery. The resting ECG (Figure 1) and chest radiograph (Figure 2) were unremarkable. A transesophageal echocardiogram showed a degenerated mitral valve with rupture of chordae tendineae and leaflet prolapse causing severe mitral regurgitation (Figure 3). Figure 1. Resting ECG. Sinus tachycardia and otherwise unremarkable findings. Figure 2. Posteroanterior and lateral chest radiograph. Normal cardiac contours and normal pulmonary vasculature and parenchyma. A vertebral prosthesis is noted. Figure 3. Preoperative transesophageal echocardiogram. Doppler image showing a wide and eccentric jet of mitral regurgitation. Preoperative computed tomographic coronary angiography demonstrated normal coronary arteries; however, all cardiac veins were found to drain into the left …

Background— β-Blockers improve clinical outcome when administered early after acute myocardial infarction. However, whether β-blockers actually reduce the myocardial infarction size is still in dispute. Cardiac magnetic resonance imaging can accurately depict the left ventricular (LV) ischemic myocardium at risk (T2-weighted hyperintense region) early after myocardial infarction, as well as the extent of necrosis (delayed gadolinium enhancement). The aim of this study was to determine whether early administration of metoprolol could increase myocardial salvage, measured as the difference between the extent of myocardium at risk and myocardial necrosis. Methods and Results— Twelve Yorkshire pigs underwent a 90-minute left anterior descending coronary occlusion, followed by reperfusion. They were randomized to metoprolol (7.5 mg during myocardial infarction) or placebo. Global and regional LV function, extent of myocardium at risk, and myocardial necrosis were quantified by cardiac magnetic resonance imaging studies performed 4 and 22 days after reperfusion in 10 survivors. Despite similar extent of myocardium at risk in metoprolol- and placebo-treated pigs (30.9% of LV versus 30.6%; P =NS), metoprolol resulted in 5-fold-larger salvaged myocardium (32.4% versus 6.2% of myocardium at risk; P =0.015). The LV ejection fraction significantly improved in metoprolol-treated pigs between days 4 and 22 (37.2% versus 43.0%; P =0.037), whereas it remained unchanged in pigs treated with placebo (35.1% versus 35.0%; P =NS). The extent of myocardial salvage was related directly to LV ejection fraction improvement ( P =0.031) and regional LV wall motion recovery ( P =0.039) at day 22. Conclusions— Early metoprolol administration during acute coronary occlusion increases myocardial salvage. The extent of myocardial salvage, measured as the difference between myocardium at risk and myocardial necrosis, was associated with regional and global LV motion improvement.

Introduction: In some circumstances left ventricular assist devices (LVAD) can be used to bridge patients with advanced heart failure to myocardial recovery or “remission”. Evaluation of the underlying myocardial function in patients supported with an LVAD is often performed with the pump speed turned down to minimal support for 15 minutes, to simulate unassisted ventricular loading conditions. Longer duration of reduced support and performance of exercise may allow for a more realistic evaluation of myocardial function to assess for recovery. Methods: Nine turn-down exams from 4 patients were analyzed. Subjects were participants in a multi-center prospective non-randomized study of LV recovery with HeartMate II LVAD together with a standardized protocol of pharmacological therapy (REmission from STAGE D Heart Failure (RESTAGE-HF)). LVEF and speckle tracking parameters were measured during full support, at 15 minutes of reduced support (6000 rpm) and again after a 6-min walk test. Averaged radial and circumferential strain, and global circumferential strain were analyzed from papillary muscle level short-axis view using speckle-tracking. Results: LV systolic parameters for each of these patients are shown, (Table). Improvement in LV function was not evident at 15 minutes of reduced support, compared to full support but was evident after the 6-min walk test. Conclusions: After 15 minutes of LVAD turndown, LV systolic parameters did not differ from full support values. Improvement in LV function compared to full support became evident when the protocol was extended to include imaging after a longer period of turndown with the addition of a 6-min walk test.

Supplemental Digital Content is available in the text, Background: The benefit of ≤6-month compared with 12-month dual antiplatelet therapy (DAPT) after percutaneous coronary intervention (PCI) with drug-eluting stent (DES) placement remains controversial. We performed a meta-analysis and meta-regression of ≤6-month versus 12-month DAPT in patients undergoing PCI with DES placement. Methods: We conducted electronic database searches of randomized controlled trials (RCTs) comparing DAPT durations after DES placement. For studies with longer follow-up, outcomes at 12 months were identified. Odds ratios and 95% confidence intervals were computed with the Mantel–Haenszel method. Fixed-effect models were used; if heterogeneity (I2) > 40 was identified, effects were obtained with random models. Results: Nine RCTs were included with total n = 19,224 patients. No significant differences were observed between ≤6-month compared with 12-month DAPT in all-cause mortality (OR 0.87; 95% confidence interval (CI): 0.69–1.11), cardiovascular (CV) mortality (OR 0.89; 95% CI: 0.66–1.21), non-CV mortality (OR 0.85; 95% 0.58–1.24), myocardial infarction (OR 1.10; 95% CI: 0.89–1.37), stroke (OR 0.97; 95% CI: 0.67–1.42), stent thrombosis (ST) (OR 1.37; 95% CI: 0.89–2.10), and target vessel revascularization (OR 0.95; 95% CI: 0.77–1.18). No significant difference in major bleeding (OR 0.72; 95% CI: 0.49–1.05) was observed, though the all-bleeding event rate was significantly lower in the ≤6-month DAPT group (OR 0.76; 95% CI: 0.59–0.96). In the meta-regression analysis, a significant association between bleeding events and non-CV mortality with 12-month DAPT was found, as well as between ST and mortality in addition to MI with ≤6-month DAPT. Conclusion: DAPT for ≤6 months is associated with similar mortality and ischemic outcomes but less bleeding events compared with 12-month DAPT after PCI with DES.

Obesity has become a national epidemic with significant implications in the development of multiple diseases. Prior studies have shown that physicians often fail to diagnose obesity in the outpatient settings, and consequently fail to formulate treatment plans and medical interventions. With the introduction of electronic medical records, making the diagnosis of obesity in an inpatient setting is a straightforward process. Our objective was to determine the presence and extent of underreporting of obesity in hospitalized patients in an urban academic medical center and to identify determinants and consequences of underreporting. We used a proprietary electronic medical record aggregator platform (Clinical Looking Glass) to collect data on all adult admissions during 2007-2010 to Montefiore Medical Center, a tertiary medical center. Presence or absence of diagnosis of obesity in patients’ problem list was identified by examining inpatient problem list in the electronic record. Our study population included 22,857 obese adults (BMI of ≥ 30 kg/m 2 ) of whom 66 % were female, 37% Black, 18.45% White, and 37.9% Hispanic. Overall, only 18.4% of the study population carried the diagnosis of obesity. There was significant variation in rates of correct diagnosis among different subgroups: 20.4% in women vs. 14.4% in men; and 22.4% in Blacks vs. 13.6% in Whites. There was a linear correlation between severity of obesity and correct diagnosis (53.38% of patients with BMI >45 kg/m 2 vs. 7.89% with BMI 30-35 kg/m 2 ) (Fig. 1). In Kaplan-Meier survival analysis, patients with correctly reported obesity demonstrated decreased mortality rates after an average follow up of two years (6.4%, CI 5.6-7.3 vs. 11.4% CI 10.9-12). In conclusion, the correct diagnosis of obesity is severely underreported in hospitalized adult patients, with race, ethnicity, gender and degree of obesity being important determinants of this observation. Correct diagnosis of obesity is associated with decreased mortality over a two-year follow-up.

Background: The aim of this study was to evaluate 2D Speckle Tracking radial strain by ultrasound in stunned and scarred myocardium as defined by cardiac magnetic resonance (CMR) in a porcine reperfusion model of acute MI. Methods: Seven pigs underwent MI induction by 90′ mid-LAD balloon occlusion. CMR was performed in a 1.5 T magnet 4 days post-MI. For edema imaging a T2-weighted sequence was employed. Delayed enhancement (DE) images were acquired 10–15 minutes after the administration of 0.2 mmol/kg of Gd-DTPA using an inversion recovery gradient-echo sequence. Before CMR, echocardiographic short axis images of the LV were obtained at the basal, mid and apical levels. Echo and CMR images were matched and divided into 6 segments per slice. DE and edema were defined as those regions with signal intensity >3 SD of the mean signal of remote normal myocardium, and quantified as % of the LV. Stunned myocardium was defined as edema- DE. Radial strain was compared in segments containing predominantly normal myocardium (25% (edema - DE); n=12] or predominantly scar (>75 % DE; n=19). Results: A total of 126 segments were analyzed. Radial strain was negatively correlated with the amount of edema (r=−0.41) and scar (r=−0.39, p ) Conclusions: Our study suggests that 2D Speckle Tracking radial strain can be a simple tool to differentiate stunned from scarred segments. This could be particularly useful in unstable patients after acute MI.

Introduction: MDCT coronary angiography has been evolving as a noninvasive method for the assessment of coronary artery disease (CAD). More recently, It has been demonstrated that MDCT identifies reduced contrast enhancement in ischemic and/or scarred myocardial segments. Objective: to determine the ability of rest-stress multidetector computed tomography (RS-MDCT) to detect myocardial ischemia and to assess the relationship between MDCT myocardial perfusion abnormalities and coronary artery stenosis. Methods: Forty seven patients underwent stress/rest 99mTc sestamibi SPECT and RS-MDCT, using a 16-row detector scanner (Philips Brilliance-16). Myocardial segments were classified by SPECT as normal, ischemic or scarred. SPECT results were then compared with MDCT regional myocardial contrast enhancement. The results of MDCT coronary angiography were also analyzed in 20 patients who underwent invasive catheterization. Results: The presence of a reduction in contrast enhancement at rest by MDCT identified scar by SPECT with 96% sensitivity and 98% specificity. A stress-induced reduction in contrast enhancement by MDCT identified ischemia by SPECT with 77% sensitivity and 99% specificity. The segment-based sensitivity and specificity for the detection of significant stenosis by MDCT were 92% and 98%, respectively. Conclusion: Our results showed that a rest-dipyridamole stress MDCT protocol can identify the presence of myocardial ischemia as well as the severity of coronary artery stenosis in patients with suspected coronary artery disease.

Background. Aortic valve stenosis (AVS) is the second most common indication for heart surgery. Althoug recent observations linked AVS and atherosclerosis, medical treatment of AVS is limited. ApoAI-Milano (ApoAI-M) is a mutant form of ApoAI. We have recently shown that ApoAI-M rapidly regressed established atherosclerotic lesions in a hypercholesteremic rabbit model. The aim of this study was to test whether hypercholestermia decreases AVA in rabbits and whether this can be reversed by short-term ApoAI-M-treatment. Methods. We used transthoracic echocardiography (Philips HD 11 XE echograph with a 12-MHz phased-array probe) to compare AVA, as determined by continuity equation, of 14 white New Zeeland rabbits, fed with atherogenic diet (0.2 % of cholesterol) for nine month, with 6 healthy controls. The hypercholesterolemic animals were then randomized into ApoAI-M (ETC-216; Pfizer): 2 injections (75mg/Kg) in 4 days, or placebo. Six days after the last dose, we assessed aortic valve morphology by echocardiography and histopathology. Results. Hypercholesteremic diet resulted in a markedly reduced AVA compared to controls (0.17±0.02cm2 vs. 0.21±0.03cm2, p Conclusion. We show that reduction of AVA can be induced experimentally in hypercholesterolemic rabbits and can be investigated by transthoracic echocardiography. In addition, this study provides for the first time evidence that AVA can be increased pharmacologically, namely by treatment with ApoAI-M.

Non-invasive assessment of plaque burden by Multislice Computed Tomography (MDCT) has been recently shown to be feasible. However, to date, there is no data on its accuracy to assess changes in atheroma burden We and others have previously shown that apoA-IMilano (apoA-IM) infusion induces a large plaque regression in a very short period of time The aim of our study was to assess the feasibility of MDCT to accurately quantify the changes in atheroma volume induced by apoA-IM infusion Methods Aortic atherosclerotic lesions were induced in New-Zealand-White Rabbits (n=7) by 9-month atherogenic diet and aortic denudation, as previously reported. Animals were then randomized to receive 2 infusions, 4 days apart, of apoA-IM (ETC-216, Pfizer. n=4) or equal volume of placebo (n=3). All animals underwent 2 imaging studies in a 64-Slice MDCT scanner (Sensation 64, Siemens), pre- and post-treatment (Rx). After last MDCT study, animals were sacrificed and the aorta processed for histological atherosclerotic lesions characterization and volume quantification . Axial MDCT images were reconstructed (3 mm thick, no overlap). Display settings were manipulated according to previous validated studies. For lumen delineation: window width (WW) 1 and level (WL) 65% of lumen attenuation . For outer vessel boundaries: WW 155% and WL 65%. Results MDCT showed that plaque burden regressed by 29% in apoA-IM group (418mm 3 pre-Rx vs. 302mm 3 post-Rx, p=0.031). Conversely, no significant change was observed by MDCT studies done pre- and post-placebo administration. MDCT performed post-Rx showed that mean plaque volume in apoA-IM animals was 11.5% smaller than that of placebo animals (p=0.018). Mean plaque volume in histology showed similar results:plaque volume was 10.6% smaller in the apoA-IM group (p=0.005 vs. placebo). The interobserver variability for plaque volume quantification in MDCT was 10±4%. Conclusion MDCT detects the changes in atherosclerotic plaque volume induced by apoA-IM infusion. Furthermore, an excellent correlation was found between MDCT and histological plaque volumes. These results, combined to the short time of scan and the accessibility to the coronary territory suggest that MDCT could be applied in human studies testing changes in coronary plaque volume.

A 43-year-old man was admitted with progressive fatigue, shortness of breath, and orthopnea. He received an orthotopic heart transplant 13 years ago, which was complicated by multiple episodes of rejection. His last catheterization 2 years before presentation demonstrated moderate transplant vasculopathy. More recently, a nuclear perfusion scan showed a myocardial scar in the mid to basal anterior and anterolateral walls, but no reversible stress-induced ischemia. On admission, the ECG showed normal …

Background Early diastolic intraventricular pressure gradients (IVPGs) have been proposed to relate to left ventricular (LV) elastic recoil and early ventricular “suction.” Animal studies have demonstrated relationships between IVPGs and systolic and diastolic indices during acute ischemia. However, data on the effects of improvements in LV function in humans and the relationship to IVPGs are lacking. Methods and Results Eight patients undergoing CABG and/or infarct exclusion surgery had a triple-sensor high-fidelity catheter placed across the mitral valve intraoperatively for simultaneous recording of left atrial (LA), basal LV, and apical LV pressures. Hemodynamic data obtained before bypass were compared with those with similar LA pressures and heart rates obtained after bypass. From each LV waveform, the time constant of LV relaxation (τ), +dP/dt max , and −dP/dt max were determined. Transesophageal echocardiography was used to determined end-diastolic (EDV) and end-systolic (ESV) volumes and ejection fractions (EF). At similar LA pressures and heart rates, IVPG increased after bypass (before bypass 1.64±0.79 mm Hg; after bypass 2.67±1.25 mm Hg; P max , −dP/dt max , and τ (each P r =−0.64) and EDV (IVPG=−0.027[EDV]+4.30, r =−0.70). Improvements in IVPGs correlated with improvements in apical τ (Δτ =5.93[ΔIVPG]+4.76, r =0.91) and basal τ (Δτ =2.41[ΔIVPG]+5.13, r =−0.67). Relative changes in IVPGs correlated with changes in ESV (ΔESV=−0.97[%ΔIVPG]+23.34, r =−0.79), EDV (ΔEDV=−1.16[%ΔIVPG]+34.92, r =−0.84), and EF (ΔEF=0.38[%ΔIVPG]−8.39, r =0.85). Conclusions Improvements in LV function also increase IVPGs. These changes in IVPGs, suggestive of increases in LV suction and elastic recoil, correlate directly with improvements in LV relaxation and ESV.