ABSTRACT
Background Methamphetamine use is associated with cardiovascular disease and significant morbidity and mortality. There is only one previous study performed on echocardiographic parameters in patients with methamphetamine cardiomyopathy. Methods We performed a retrospective review of medical records in a county hospital in Southern California with a high population of methamphetamine users. We reviewed medical records and echocardiogram findings in patients seen in our institution from November 2019 to November 2020 who had cardiomyopathy with and without methamphetamine use. We excluded patients who either left the hospital or expired before appropriate assessment. We divided our patient population into a case group (methamphetamine users) and a control group (non-methamphetamine users) to study and compare their echocardiographic parameters. Results Case group included a total of 254 patients and control group included 268 patients. Majority of the patient population were males - 178 (70%) and 180 (67%) in the case and control group respectively. Age was found to be statistically significant with the younger population in the case group (p = 0.0000). Our analysis revealed statistically significant difference in methamphetamine users compared to non-users in regards to left ventricle ejection fraction (33.65% ± 18.02 vs. 41.55% ± 15.61, p=0.0000), left ventricle mass index (122.49 grams/m2 ± 40.66 vs. 108.62 grams/m2 ± 32.82, p=0.0000), left ventricle end diastolic volume index (85.91 mL/m2 ± 37.40 vs. 72.44 mL/m2 ± 25.44; p=0.0000) and marginally significant right ventricle systolic pressure (42.29mmHg ± 17.53 vs. 39.59mmHg ± 15.61; p=0.0540) Conclusion Our results indicated that methamphetamine users had echocardiogram findings with decreased ejection fraction and increased left ventricular mass index, end-diastolic volume index, and right ventricular systolic pressure consistent with worse dilated cardiomyopathy comparison to non-users.
ABSTRACT
Hypertrophic cardiomyopathy (HCM) is a common disease that can be acquired due to chronic hypertension or via autosomal dominant inheritance. Several patterns of HCM have been described, of which a rare variant is apical hypertrophic cardiomyopathy (AHCM). Atrial thrombus is a well-recognized complication of HCM especially in the setting of atrial fibrillation (AF). However, left ventricular thrombus (LVT) formation is not nearly as prevalent as atrial thrombus. Here is a case of a 57-year-old Hispanic female with AHCM who presented with significant unintentional weight loss and unexplained anemia and was subsequently found to have a large left intraventricular mass suspicious for a tumor vs. ventricular thrombus. The diagnosis was complicated due to the large size of the mass and presenting symptoms suspicious of malignancy.
ABSTRACT
BACKGROUND: This study investigates erythrocyte insulin receptor binding and affinity in subjects with hypertension and hyperinsulinemia. Insulin receptor-binding function has not been extensively studied in hypertensive subjects. METHODS: Insulin receptor density, binding affinity, and protein tyrosine kinase activity were measured in erythrocytes from 18 hypertensive and 16 normotensive subjects. Insulin sensitivity was measured by the fasting plasma insulin/glucose ratio and the homeostatic assessment model algorithm (HOMA) index. Erythrocyte insulin binding was determined by a competitive binding assay and protein tyrosine kinase activity was measured by an enzyme-linked immunoabsorbent assay technique. RESULTS: Fasting plasma insulin/glucose ratio and the insulin resistance index (HOMA) were significantly higher in the hypertensive versus normotensive subjects. Receptor saturation of the high affinity binding sites (Bmax) was reduced in the hypertensive versus control subjects. The Kd values were lower in the erythrocytes from hypertensive than control subjects. Insulin-induced protein tyrosine kinase activity was decreased in erythrocytes from hypertensive versus control subjects. CONCLUSIONS: A reduced erythrocyte insulin receptor density and tyrosine protein kinase activity may reflect insulin receptor dysfunction in hypertensive individuals who have insulin resistance and hyperinsulinemia. More information is needed examining insulin receptor function in other target tissues such as fat or skeletal muscle cells before defects in the insulin receptor can be firmly proposed as a cause of the metabolic syndrome.
