The inverse relationship between high-density lipoprotein cholesterol (HDL-C) concentrations and coronary heart disease risk is well established. As a result, in recent years there have been significant resources focused on identifying therapies that raise HDL-C and ultimately reduce cardiovascular events. Unfortunately, a number of trials aimed at increasing HDL-C have failed to show improved outcomes, and hence, have cast doubt on the importance of HDL-C as a therapeutic target. HDL-C, however, is only one measure of HDL. HDL levels can also been estimated by quantifying apolipoprotein A-I (apoA-I) levels using enzyme immunoassay or by measuring HDL particle number (HDL-P) using nuclear magnetic resonance spectroscopy (NMR) or ion mobility. While these surrogate measures are correlated, they are not comparable. Lipoprotein-altering therapies have been shown to have different effects on HDL-C, apoA-I and HDL-P and several studies have demonstrated that HDL-P is a stronger predictor of coronary heart disease risk than HDL-C and/or apoA-I. This paper will review available evidence supporting the use of HDL-P as the biomarker of choice to assess the contribution of HDL to cardiovascular risk and as the primary goal of HDL-raising therapies.
Summary:Malignant nonseminomatous germ cell tumors (NSGCT) rarely metastasize to the heart. The first such case presenting with syncope is described. Eight previously described cases of NSGCT with intracaval metastasis to the heart are reviewed and the literature to date is discussed. Transesophageal echocardiography is the diagnostic study of choice and treatment consists primarily of platinum-based chemotherapy followed by surgical resection of residual deposits.
Background:
More effective tactics are needed to evaluate patients with suspected symptomatic obstructive coronary artery disease (CAD). Results from recent studies such as PROMISE demonstrated that < 10% of these patients had a cardiac cause for their symptoms. A previously validated blood-based test, incorporating age, sex, and gene expression levels, demonstrated a 96% negative predictive value among symptomatic, non-diabetic patients in the evaluation of obstructive CAD at a threshold score of 15 or less, where a low score is indicative of low likelihood of obstructive CAD.
Objective:
The objective of this retrospective, case-control study (NCT02223286) was to evaluate the use of an age/sex/gene expression score (ASGES) and conventional anatomic and functional testing in the diagnostic work-up of patients referred for assessment of stable symptoms suggestive of obstructive CAD in the cardiologist’s office.
Methods:
In this post-hoc case series analysis, patients with stable symptoms suggestive of obstructive CAD referred to two cardiologists underwent both ASGES (range 1-40) testing and additional cardiac testing, which included ETT, stress echo, MPI, or CCTA. Demographics and clinical factors as well as ASGES results (predefined as low score/low likelihood of obstructive CAD [ASGES ≤15] or elevated score/elevated likelihood of obstructive CAD [ASGES >15]) and other cardiac test results were collected.
Results:
Among 67 patients in this analysis, the mean age was 52 years, 60% of the patients were female, 30% were smokers, 54% had hypertension, and 60% had dyslipidemia. The mean ASGES score was 13, and 63% (42/67) of the patients had an ASGES ≤15 (low score). Upon additional cardiac testing, 0% (0/42) of patients with a low score as compared to 20% (5/25) of patients with an elevated score had at least one abnormal anatomical or functional cardiac test result (p<0.01).
Conclusion:
In this case series analysis, utilization of additional cardiac testing in low ASGES patients did not add new information for further clinical-decision making. Based on these findings, a strategy of using the ASGES test early in the diagnostic process may lead to a reduction of further cardiac testing among low ASGES patients who have a low likelihood of obstructive CAD.
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