Giant Cell Myocarditis Following COVID-19 Successfully Treated by Immunosuppressive Therapy

In this case report, we present a 46-year-old lady who has developed a rapidly progressive heart failure after an episode of COVID-19. The pathologic examination of her endomyocardial biopsy specimens was compatible with GCM and she was successfully treated with a combined immunosuppressive therapy regimen.

Dilated Cardiomyopathy in Children and Adolescents in the South Region of Kyrgyzstan

Research relevance: in recent decades, there has been a significant increase in interest in cardiomyopathies, mainly of the heart muscle, often characterized by an unclear etiology, chronic progressive course and, ultimately, cardiomegaly, progressive heart failure, arrhythmic, thromboembolic syndromes, often ending in sudden cardiac death. Materials and research methods: presentation of results after statistical studies on the clinic, diagnostics of a violation of the conducting system by cardiomyopathy in children aged 1 to 16 years, who underwent inpatient treatment in the cardioreumatology department of the Osh medical children’s clinical hospital from 2016 to 2020, according to clinical material on 67 children with dilated cardiomyopathy. Research objectives: analysis of data on 67 children from 0 to 16 years old who received inpatient treatment for heart disease at the Osh interregional children's clinical hospital from 2016 to 2020. Research results: analysis of the EchoCG data of the study showed that the nature of changes in intracardiac hemodynamics depends on the age of the child: the most pronounced shifts in EchoCG indicators, as a rule, are inherent in young children with inflammatory changes in the myocardium and dilated cardiomyopathy, less pronounced for children of other age groups. Conclusions: indicators reflect severe degree of heart damage in children of this age and indicate, most likely, a weak level of heart compensatory-adaptive mechanisms.

Adult Obstructive Cor Triatriatum with Severe Mitral Regurgitation: A Case Report

Adult cor triatriatum sinister associated with severe mitral regurgitation is extremely rare. As these obstructive cor triatriatum feature hemodynamics that mimic mitral stenosis, a pressure load is theoretically generated only on the left atrial proximal chamber, and therefore the left ventricle is less likely to suffer volume loading. Here, we report a surgical case with such rare hemodynamics. A 22-year-old man with obstructive cor triatriatum and severe mitral regurgitation received an anomalous membrane excision and mitral annuloplasty. An abnormal membrane with an orifice 7 mm in size was completely resected while a grossly dilated mitral annulus was repaired via annuloplasty ring. Mitral regurgitation was controlled well, and the postoperative course was uneventful. Even with obstructive cor triatriatum, severe mitral annular dilatation and subsequent left ventricular dilatation may occur, causing the progressive heart failure encountered in this case.

Mildly Increased Renin Expression in the Absence of Kidney Injury in the Murine Transverse Aortic Constriction Model

Cardiorenal syndrome type 2 is characterized by kidney failure as a consequence of heart failure that affects >50% of heart failure patients. Murine transverse aortic constriction (TAC) is a heart failure model, where pressure overload is induced on the heart without any systemic hypertension or its consequences. Whether renal function is altered in this model is debated, and if so, at which time post-TAC renal dysfunction starts to contribute to worsening of cardiac function. We therefore studied the effects of progressive heart failure development on kidney function in the absence of chronically elevated systemic blood pressure and renal perfusion pressure. C57BL/6J mice (N = 129) were exposed to TAC using a minimally invasive technique and followed from 3 to 70 days post-TAC. Cardiac function was determined with 3D ultrasound and showed a gradual decrease in stroke volume over time. Renal renin expression and plasma renin concentration increased with progressive heart failure, suggesting hypoperfusion of the kidney. In addition, plasma urea concentration, a surrogate marker for renal dysfunction, was increased post-TAC. However, no structural abnormalities in the kidney, nor albuminuria were present at any time-point post-TAC. Progressive heart failure is associated with increased renin expression, but only mildly affected renal function without inducing structural injury. In combination, these data suggest that heart failure alone does not contribute to kidney dysfunction in mice.

Left Ventricular Non-Compaction Cardiomyopathy, Ventricular Septal Defect and Pre-excitation: A Rare Coexistence of Three Abnormities in an Adult Patient.

A congenital cardiac condition characterized by ventricular trabeculations and intertrabecular recesses is described as a non-compaction cardiomyopathy. In clinical practice, since it can be associated with severe mortality and morbidity due to progressive heart failure, thromboembolic events, and fatal arrhythmias, it is important to consider non-compaction cardiomyopathy. In this case, we have an adult patient who underwent surgery due to a ventricular septal defect (VSD) and who was later diagnosed with left ventricular non-compaction cardiomyopathy (LVNC) and pre-excitation. To our knowledge, this is the first case of VSD, LVNC, and pre-excitation simultaneously present in an adult patient.

Exploring the complex interplay in the regulation of cardiac pathophysiological functions by protein kinases and phosphatases

Cardiovascular disease manifests as an intricately complex entity presenting as a derangement of the cardiovascular system. Cardiac or heart failure connotes the pathophysiological state in which deficient cardiac output compromises the body burden and requirements. Protein kinases regulate several pathophysiological processes and are emerging targets for drug lead or discovery. The protein kinases are family members of the serine/threonine phosphatases. Protein kinases and phosphatases are pivotal in the regulatory mechanisms in the reversible phosphorylation of diverse effectors whereby discrete signaling molecules regulate cardiac excitation and contraction. Protein phosphorylation is critical for the sustenance of cardiac functionalities. The two major contributory ingredients to progressive myocardium derangement are dysregulation of Ca2+processes and contemporaneous elevated concentrations of reactive oxygen species, ROS. Certain cardiac abnormalities include cardiac myopathy or hypertrophy due to response in untoward haemodynamic demand with concomitant progressive heart failure. The homeostasis or equilibrium between protein kinases and phosphatases influence cardiac morphology and excitability during pathological and physiological processes of the cardiovascular system.

Abstract 17341: Obesity is Associated With Progressive Heart Failure in Hypertrophic Cardiomyopathy

Background: The impact of comorbid disease states and lifestyle on the natural history of patients with hypertrophic cardiomyopathy (HCM) remains unknown. Objective: Evaluate the association of non-HCM comorbidities including obesity, hypertension, diabetes, obstructive sleep apnea, kidney disease, tobacco use, alcohol use, and lung disease with disease progression in a large cohort of HCM patients. Methods: 2269 patients evaluated at the Tufts HCM Institute between 2004 to 2019, ≥ 18 years of age (54 ± 15 years; 1392 male), and followed for an average of 4 ± 3.4 years for disease progression including progressive heart failure (HF) symptoms (from NYHA class I/II to NYHA class III/IV), new-onset atrial fibrillation (AF), or sudden death (SD) event (including appropriate defibrillation for ventricular arrhythmias, resuscitated cardiac arrest, or SD). Results: Of 1376 patients with NYHA class I/II symptoms at initial clinical evaluation, 252 (18%) developed progressive HF symptoms to NYHA class III/IV over follow-up (5%/year). Obesity (BMI ≥ 30) was significantly more prevalent in patients who had progressive HF during follow-up (43%) compared to those who remained without HF (34%, p = 0.014). In contrast, other comorbidities were not significantly associated with progressive HF symptoms (p > 0.10 for all other comorbidities). Of the 1823 patients without AF history at initial clinical visit, 198 (11%) developed new-onset AF over follow-up (3%/year). No comorbidities were significantly associated with new-onset AF in HCM (p > 0.10), although obesity was more common in patients who developed new-onset AF (48%) compared to those who had no AF (41%, p = 0.08). Notably, SD events were not associated with non-HCM comorbidities (p > 0.10 for all comorbidities), and patients with SD events were less likely to have comorbidities than patients without SD events. Conclusions: In adult HCM patients, obesity is associated with progressive symptoms and outcomes supporting weight loss as an important modifier in obese HCM patients to potentially help prevent HCM complications. In contrast, other non-HCM comorbidities do not appear to impact disease course, and SD events are not associated with comorbidities in HCM.