Coronary artery disease is present in 40-55% of patients with diastolic heart failure, and myocardial ischemia is both a cause and a precipitant of diastolic heart failure. Failure to recognize and treat acute and chronic ischemia in patients with this disorder results in rapid disease progression and poor outcomes. In diastolic heart failure patients without obstructive coronary artery disease, ischemia can be induced by other diseases that diminish perfusion gradient, cause myocardium to outgrow blood supply, or decrease diastolic filling time. In this article, we review the role of ischemia and development of fibrosis in the epidemiology, pathophysiology, and evaluation of patients with diastolic dysfunction and diastolic heart failure.
Morbid obesity is believed to limit cardiovascular auscultation. We compared audiocardiography to senior attending physicians using conventional stethoscopes in 190 individuals with morbid obesity. Overall, there were 128 (67.4%) women and 62 (32.6%) men with mean ages of 44.9 +/- 12.3 and 51.3 +/- 10.8 , respectively (P = 0.001). The overall body mass index (BMI) was 47.3 +/- 8.5 kg m(-2). Of those with an S(3) by audiocardiography (n = 7), one had a history of coronary artery disease (CAD), none had a history of heart failure, and one had a left ventricular ejection fraction (LVEF) <45%. The mean LVEF was 58.6 +/- 9.9 versus 61.6 +/- 5.3 for those with and without an S(3) by audiocardiography (P = 0.16). By contrast, of those (n = 6) with an S(3) by stethoscope, one had a history of CAD, two had histories of heart failure, and 3 had LVEF < 45%. The mean LVEF of those with and without S(3) by stethoscope was 53.7 +/- 2.3 and 61.6 +/- 5.5%, respectively (P = 0.02). There were 40 (21.1%) patients with an S(4) (S(4) strength >5) identified by acoustic cardiography while there were 42 (22.1%) heard by the stethoscope and it was heard with both methods in nine patients (21.4% concordance). There were no significant correlations between BMI or peak oxygen consumption and S(3) or S(4) strength by audiocardiography. Acoustic cardiography performed with an electronic device was not helpful in assisting the cardiovascular examination of the morbidly obese. These data suggest the careful clinical exam with attention to traditional cardiac auscultation using a stethoscope in a quiet room should remain the gold standard.
As more patients recover from COVID-19 infection, long-term complications are beginning to arise. Our case report will explore a debilitating long-term complication, Post-COVID Interstitial Lung Disease (PC-ILD). We will introduce a patient who developed PC-ILD in the setting of diffuse large B-cell lymphoma, outlining a difficult hospital course, including a positive COVID-19 polymerase chain reaction (PCR) for more than 3 months. We will then discuss the human body’s physiological response to the virus and how our patient was not able to adequately mount an immune response. Finally, the pathophysiology of PC-ILD will be explored and correlated with the patient’s subsequent computed tomographic images obtained over a 3-month period. The difficult hospital course and complex medical decision-making outlined in this case report serve as a reminder for health care providers to maintain vigilance in protecting our most vulnerable patient population from such a devastating disease process.
Amyloidosis is a rare disease with an incidence of only 16.6 per 100,000 patients per year. A high grade of clinical suspicion is required to suspect an atypical cause of left ventricular hypertrophy or new-onset heart failure. A transthoracic echocardiogram (TTE) is the initial evaluation that may yield clues pointing towards an etiology of cardiac amyloidosis. Due to the subjective nature of TTE interpretations, suspicion for cardiac amyloidosis may be missed. Once suspicion arises, additional tests, such as serum and urine electrophoresis and technetium-99m pyrophosphate myocardial perfusion imaging, can further aid in establishing a diagnosis. The pathophysiology in transthyretin amyloidosis (ATTR) involves the misfolding of the transthyretin/prealbumin protein, which leads to an inherent propensity to aggregate. These proteins can accumulate in the extracellular space between cardiac myocytes, which may thicken sections of the heart, leading to ventricular restriction. Here, we explore the case of an 83-year-old man with chronic, treatmentresistant heart failure with preserved ejection fraction, New York Heart Association class III, who presented with multiple ruptured bullae in the bilateral lower extremity, leading to a new diagnosis of ATTR cardiac amyloidosis.
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