Heartbeats in Distress: Unveiling Cardiac Sarcoidosis Through Palpitations.

Cardiac sarcoidosis (CS), a rare complication of systemic sarcoidosis, can have subtle or no symptoms. It is characterized by granuloma formation in the myocardium, which can occur in isolation or alongside systemic sarcoidosis. Clinical manifestations include conduction system disorders (e.g., atrioventricular block and ventricular tachyarrhythmia), heart failure, and sudden cardiac death. Timely evaluation and screening for CS are crucial, especially in systemic sarcoidosis patients with limited symptoms. We present the case of a 50-year-old African-American male diagnosed with cardiac sarcoidosis following a recent diagnosis of pulmonary sarcoidosis after experiencing tachycardia for two years, as confirmed by imaging studies.

Heart disease in Friedreich's ataxia.

Friedreich's ataxia (FRDA), which occurs in 1/50000 live births, is the most prevalent inherited neuromuscular disorder. Nearly all FRDA patients develop cardiomyopathy at some point in their lives. The clinical manifestations of FRDA include ataxia of the limbs and trunk, dysarthria, diabetes mellitus, and cardiac diseases. However, the broad clinical spectrum makes FRDA difficult to identify. The diagnosis of FRDA is based on the presence of suspicious clinical factors, the use of the Harding criteria and, more recently, the use of genetic testing for identifying the expansion of a triplet nucleotide sequence. FRDA is linked to a defect in the mitochondrial protein frataxin; an epigenetic alteration interferes with the folding of this protein, causing a relative deficiency of frataxin in affected patients. Frataxins are small essential proteins whose deficiency causes a range of metabolic disturbances, including oxidative stress, iron-sulfur cluster deficits, and defects in heme synthesis, sulfur amino acid metabolism, energy metabolism, stress responses, and mitochondrial function. The cardiac involvement seen in FRDA is a consequence of mitochondrial proliferation as well as the loss of contractile proteins and the subsequent development of myocardial fibrosis. The walls of the left ventricle become thickened, and different phenotypic manifestations are seen, including concentric or asymmetric hypertrophy and (less commonly) dilated cardiomyopathy. Dilated cardiomyopathy and arrhythmia are associated with mortality in patients with FRDA, whereas hypertrophic cardiomyopathy is not. Systolic function tends to be low-normal in FRDA patients, with an acute decline at the end of life. However, the literature includes only a few long-term prospective studies of cardiac progression in FRDA, and the cause of death is often attributed to heart failure and arrhythmia postmortem. Cardiomyopathy tends to be correlated with the clinical neurologic age of onset and the nucleotide triplet repeat length (i.e., markers of phenotypic disease severity) rather than the duration of disease or the severity of neurologic symptoms. As most patients are wheelchair-bound within 15 years of diagnosis, the clinical determination of cardiac involvement is often complicated by comorbidities. Researchers are currently testing targeted therapies for FRDA, and a centralized database, patient registry, and natural history study have been launched to support these clinical trials. The present review discusses the pathogenesis, clinical manifestations, and spectrum of cardiac disease in FRDA patients and then introduces gene-targeted and pathology-specific therapies as well as screening guidelines that should be used to monitor cardiac disease in this mitochondrial disorder.

Delayed Chronotropic Response due to Autonomic Imbalance Presenting as Dyspnea on Early Exertion: A Complication of Bariatric Surgery.

Bariatric surgery has shown promising outcomes in improving overall morbidity and mortality in morbidly obese patients. Cardiovascular risk reduction from weight loss is well known in the literature. However, little is highlighted about the cardiovascular complications of massive and rapid weight loss associated with bariatric surgery. These complications result mainly from autonomic imbalance manifesting as increased parasympathetic tone and a decrease in sympathetic response. This imbalance is a consequence of hormonal changes associated with massive weight loss. We present a unique case which is a demonstration of the aforementioned changes. Our patient presented with dyspnea during an early phase of exercise with the resolution of symptoms with the continuation of exercise.