Pericardial Disease in Cardiac Amyloidosis: A Comprehensive Review.

In patients with cardiac amyloidosis, pericardial involvement is common, with up to half of patients presenting with pericardial effusions. The pathophysiological mechanisms of pericardial pathology in cardiac amyloidosis include chronic elevations in right-sided filling pressures, myocardial and pericardial inflammation due to cytotoxic effects of amyloid deposits, and renal involvement with subsequent uremia and hypoalbuminemia. The pericardial effusions are typically small; however, several cases of life-threatening cardiac tamponade with hemorrhagic effusions have been described as a presenting clinical scenario. Constrictive pericarditis can also occur due to amyloidosis and its identification presents a clinical challenge in patients with cardiac amyloidosis who concurrently manifest signs of restrictive cardiomyopathy. Multimodality imaging, including echocardiography, cardiac computed tomography, and cardiac magnetic resonance imaging, is useful in the evaluation and management of this patient population. The recognition of pericardial effusion is important in the risk stratification of patients with cardiac amyloidosis as its presence confers a poor prognosis. However, specific treatment aimed at the effusions themselves is seldom indicated. Cardiac tamponade and constrictive pericarditis may necessitate pericardiocentesis and pericardiectomy, respectively.

The Obesity Mortality Paradox in Patients with Pulmonary Embolism: Insights from a Tertiary Care Center.

Background: While obesity is associated with an increased risk of venous thromboembolism (VTE), there is some data to suggest that higher BMI is also associated with decreased all-cause mortality in patients with a pulmonary embolism (PE). Methods: Using PE Response Team (PERT) activation data from a large tertiary hospital between 27 October 2020 and 28 August 2023, we constructed a multivariate Cox proportional hazards model to assess the association between obesity as a dichotomous variable (defined as BMI ≥ 30 vs. BMI 18.5-29.9), BMI as a continuous variable, and 30-day PE-related mortality. Results: A total of 248 patients were included in this analysis (150 with obesity and 98 who were in the normal/overweight category). Obesity was associated with a lower risk of 30-day PE-related mortality (adjusted HR 0.29, p = 0.036, 95% CI 0.09-0.92). A higher BMI was paradoxically associated with a lower risk of PE-related mortality (HR = 0.91 per 1 kg/m2 increase, p = 0.049, 95% CI 0.83-0.999). Conclusions: In our contemporary cohort of patients with a PERT activation, obesity was associated with a lower risk of PE-related mortality.

Current and emerging pharmacotherapy for the management of hypertrophic cardiomyopathy.

INTRODUCTION: Hypertrophic cardiomyopathy (HCM) is one of the most common genetic causes of heart disease. Since the initial description of HCM, there have been minimal strides in management options. Obstructive HCM constitutes a larger subset of patients with increased left ventricular outflow tract gradients causing symptoms. Septal reduction therapy (SRT) has been successful, but it is not the answer for all patients and is not disease modifying. AREAS COVERED: Current guideline recommendations include beta-blockers, calcium channel blockers, or disopyramides for medical management, but there lacks evidence of much benefit with these drugs. In recent years, there has been the emergence of cardiac myosin inhibitors (CMI) which have demonstrated positive results in patients with both obstructive and non-obstructive HCM. In addition to CMIs, other drugs have been investigated as we have learned more about HCM's pathological mechanisms. Drugs targeting sodium channels and myocardial energetics, as well as repurposed drugs that have demonstrated positive remodeling are being investigated as potential therapeutic targets. Gene therapy is being explored with vast potential for the treatment of HCM. EXPERT OPINION: The armamentarium of therapeutic options for HCM is continuously increasing with the emergence of CMIs as mainstays of treatment. The future of HCM treatment is promising.

Nationwide Analysis of Cardiac Arrest Outcomes During the COVID-19 Pandemic.

The coronavirus disease 2019 (COVID-19) pandemic had a significant impact on the chain of survival following cardiac arrest. However, large population-based reports of COVID-19 in patients hospitalized after cardiac arrest are limited. The National Inpatient Sample database was queried for cardiac arrest admissions during 2020 in the United States. Propensity score matching was used to match patients with and without concurrent COVID-19 according to age, race, sex, and comorbidities. Multivariate logistic regression analysis was used to identify predictors of mortality. A weighted total of 267,845 hospitalizations for cardiac arrest were identified, among which 44,105 patients (16.5%) had a concomitant diagnosis of COVID-19. After propensity matching, cardiac arrest patients with concomitant COVID-19 had higher rate of acute kidney injury requiring dialysis (64.9% vs 54.8%) mechanical ventilation >24 hours (53.6% vs 44.6%) and sepsis (59.4% vs 40.4%) compared to cardiac arrest patients without COVID-19. In contrast, cardiac arrest patients with COVID-19 had lower rates of cardiogenic shock (3.2% vs 5.4%, P < 0.001), ventricular tachycardia (9.6% vs 11.7%, P < 0.001), and ventricular fibrillation (6.7% vs 10.8%, P < 0.001), and a lower utilization of cardiac procedures. In-hospital mortality was higher in patients with COVID-19 (86.9% vs 65.5%, P < 0.001) and, on multivariate analysis, a diagnosis of COVID-19 was an independent predictor of mortality. Among patients hospitalized following a cardiac arrest during 2020, concomitant COVID-19 infection was associated with significantly worse outcomes characterized by an increased risk of sepsis, pulmonary and renal dysfunction, and death.

Nonalcoholic Fatty Liver Disease and Cardiovascular Disease: Causation or Association.

Nonalcoholic fatty liver disease (NAFLD) is a disease process that is gaining increasing recognition. The global prevalence of NAFLD is increasing in parallel with growing rates of risk factors for NAFLD such as hypertension, obesity, diabetes, and metabolic syndrome. NAFLD has been referred to as a risk factor for cardiovascular disease (CVD). As CVD is the leading cause of morbidity and mortality worldwide, there are constant efforts to describe and alleviate its risk factors. Although there is conflicting data supporting NAFLD as a causative or associative factor for CVD, NAFLD has been shown to be associated with structural, electrical, and atherosclerotic disease processes of the heart. Shared risk factors and pathophysiologic mechanisms between NAFLD and CVD warrant further explication. Pathologic mechanisms such as endothelial dysfunction, oxidative stress, insulin resistance, genetic underpinnings, and gut microbiota dysregulation have been described in both CVD and NAFLD. The mainstay of treatment for NAFLD is lifestyle intervention including physical exercise and hypocaloric intake in addition to bariatric surgery. Investigations into various therapeutic targets to alleviate hepatic steatosis and fibrosis by way of maintaining the balance between lipid synthesis and breakdown. A major obstacle preventing the success of many pharmacologic approaches has been the effects of these medications on CVD risk. The future of pharmacologic treatment of NAFLD is promising as effective medications with limited CVD harm are being investigated.

Hyperlipidemia in Children and Adolescents.

While coronary artery disease (CAD) is thought to be a disease of adulthood, atherosclerosis can originate in childhood and adolescence. There is a paucity of randomized controlled treatment trials regarding dyslipidemia among the younger population. However, it is apparent that childhood dyslipidemia is associated with an earlier onset of CAD. Most recent guidelines by the American College of Cardiology (ACC) and American Heart Association (AHA) focus on lifestyle modification and lifetime risk of atherosclerotic disease, as well as adequate screening measures. Genetic factors, environmental contributors such as pollution, obesity linked to poor nutrition, and sedentary lifestyles are shown to be associated with increased lipid levels and early CAD among children and adolescents. Familial hyperlipidemia is one of the most prevalent genetic diseases and can affect 1 in 250 individuals. A multimodal treatment plan is most effective for children and adolescents with dyslipidemia including lifestyle changes (a modified diet and moderate physical activity) and pharmacologic intervention. The mainstay of pharmacologic treatment for childhood dyslipidemia is similar to that of adults. Statins are the most widely used medications. Newer medications have proven integral in treatment for genetic dyslipidemias including evolocumab and evinacumab.

Minimalist transcatheter aortic valve replacement misses paravalvular regurgitation: Incidence and echocardiographic distribution of missed paravalvular regurgitation.

BACKGROUND: Paravalvular regurgitation (PVR) may be missed intraoperatively with transthoracic echocardiography (TTE) guided minimalist TAVR. We sought to determine the incidence and echocardiographic distribution of PVR missed on intra-op TTE, but detected on predischarge TTE. METHODS: From July 2015 to 2020, 475 patients with symptomatic severe native aortic stenosis underwent TTE-guided minimalist TAVR. Missed PVR was defined as predischarge PVR that was ≥1 grade higher than the corresponding intra-op PVR severity. PVR was classified as anterior or posterior on the four standard TTE views; parasternal short-axis (PSAX), parasternal long-axis (PLAX), apical 3-chamber (A3C), and 5-chamber (A5C). Location-specific risk of missed PVR was then determined. RESULTS: Mild or greater PVR was seen in 55 (11.5%) cases intra-op and 91 (19.1%) at predischarge, with no severe PVR. Among the 91 patients with ≥mild predischarge PVR, missed PVR was present in 42 (46.2%). Compared to the corresponding anterior jets, missed PVR rate was significantly higher for posterior jets in PLAX (62.5% vs. 25.0%, p = 0.005), A5C (56.9% vs. 25.0%, p = 0.009), PSAX (66.7% vs. 24.3%, 0.001), but not A3C (58.5% vs. 40.0%, p = 0.28). CONCLUSIONS: Intraoperative TTE-guided minimalist TAVR either misses nearly half of ≥mild PVR or underestimates PVR by ≥1 grade when compared to predischarge TTE. Posterior PVR jets are more likely to be missed. Transesophageal echo guidance may help minimize missing PVR. Further studies are warranted.

MitraClip for Severe Mitral Regurgitation from Chordal Rupture during Balloon Aortic Valvuloplasty.

Transcatheter aortic valve replacement (TAVR) has become an established alternative to surgical aortic valve replacement for high-, intermediate-, and low-risk patients. Paravalvular leak (PVL) is a complication of TAVR that can be effectively treated with balloon dilation and vascular plugs. We report a case of an 86-year-old male presenting with symptomatic severe aortic stenosis. After the index TAVR procedure, mild-to-moderate PVL was noted. Two years post-operation, the patient presented with symptomatic severe PVL, which was initially treated by balloon dilation with additional volume. During balloon dilation, the balloon slipped into the left ventricle and tore a chord, leading to new severe mitral regurgitation (MR) while the PVL remained unchanged. Subsequently, an Amplatzer vascular plug II (Abbott) was successfully used to reduce the PVL to mild, and a MitraClip NTR (Abbott) was used to successfully reduce the MR to trivial. Although balloon dilation can be an effective method for reducing PVL, mitral valve chordal rupture is a rare complication if the wire is entrapped in the chordae and the balloon slips into the ventricle.