Cardiac Amyloidosis: A Contemporary Review of Medical and Surgical Therapy.

Amyloidosis is a systemic disease initiated by deposition of misfolded proteins in the extracellular space, due to which multiple organs may be affected concomitantly. Cardiac amyloidosis, however, remains a major cause of morbidity and mortality in this population due to infiltrative /restrictive cardiomyopathy. This review attempts to focus on contemporary medical and surgical therapies for the different types of cardiac amyloidosis. Amyloidosis affecting the heart are predominantly of the transthyretin type (acquired in the older or genetic in the younger patients), and the monoclonal immunoglobulin light chain (AL) type which is solely acquired. A rare form of secondary amyloidosis AA type can also affect the heart due to excessive production and accumulation of the acute-phase protein called Serum Amyloid A" (SAA) in the setting of chronic inflammation, cancers or autoinflammatory disease. More commonly AA amyloidosis is seen in the liver and kidney. Other rare types are Apo A1 and Isolated Atrial Amyloidosis (AANF). Medical therapies have made important strides in the clinical management of the two common types of cardiac amyloidosis. Surgical therapies such as mechanical circulatory support and cardiac transplantation should be considered in appropriate patients. Future research using AI driven algorithms for early diagnosis and treatment as well as development of newer genetic engineering technologies will drive improvements in diagnosis, treatment and patient outcomes.

NT-proBNP and D-Dimer in acute decompensated heart failure: assessment of diagnostic accuracy and correlation with echocardiographic parameters.

PURPOSE: Abnormalities in coagulation and inflammation exist in heart failure. This study compares the diagnostic accuracy of NT-proBNP and D-Dimer and the correlation of these biomarkers with echocardiographic parameters in acute decompensated heart failure. METHODS: A retrospective cross-sectional/observational study was performed using 162 patients with acute decompensated heart failure and 253 age-matched controls. Patients were ruled out for a pulmonary embolus by CT or VQ scans. The study protocol was approved by Institutional Review Board, Lubbock, TX. Correlation of NT-proBNP and D-Dimer values was done with echocardiographic parameters. Statistical significance was assumed at p < 0.05. RESULTS: D-Dimer showed a positive correlation with NT-proBNP (r = 0.665, p = 001). The AUC for NT-proBNP, D-Dimer and a combination of D-Dimer plus NT-proBNP were 0.963, 0.928 and 0.982 respectively. The AUC value for D-Dimer versus the combination of D-Dimer and NT-roBNP was not significant (p = 0.21). Correlation of NT-proBNP was significant with the echocardiographic parameters but D-Dimer did not significantly correlate with any of the echocardiographic parameters studied. CONCLUSIONS: Comparison of the AUC values for D-Dimer versus the combination of D-Dimer and NT-proBNP showed no significance suggestive of comparable diagnostic accuracy in the study population. The lack of correlation between D-Dimer and echocardiographic parameters suggests an independent pathophysiological mechanism underlying upregulation of D-Dimer in acute decompensated heart failure. Further systematic studies are needed to define mechanism of D-Dimer increase in heart failure.

Cardiovascular Changes in Menopause.

Menopause is associated with changes consistent with cardiovascular aging. The effects of cardiac disease are multifaceted, affecting endothelial function, coronary artery physiology and metabolic dysfunction leading to structural changes in the coronary anatomy. A systematic review of literature from 1986 to 2019 was conducted using PubMed and Google Scholar. The search was directed to retrieve papers that addressed the changes in cardiovascular physiology in menopause and the current therapies available to treat cardiovascular manifestations of menopause. The metabolic and clinical factors secondary to menopause, such as dyslipidemia, insulin resistance, fat redistribution and systemic hypertension, contribute to the accelerated risk for cardiovascular aging and disease. Atherosclerosis appears to be the end result of the interaction between cardiovascular risk factors and their accentuation during the perimenopausal period. Additionally, complex interactions between oxidative stress and levels of L-arginine and ADMA may also influence endothelial dysfunction in menopause. The increased cardiovascular risk in menopause stems from the exaggerated effects of changing physiology on the cardiovascular system affecting peripheral, cardiac and cerebrovascular beds. The differential effects of menopause on cardiovascular disease at the subclinical, biochemical and molecular levels form the highlights of this review.