Sex Disparities in Cardiovascular Disease.

Cardiovascular disease is the leading cause of death in women. It remains underdiagnosed, undertreated, and portends worse outcomes in women than men. Disparities exist in every stage of science, from bench research to the editorial board of major journals and in every cardiovascular subspecialty. This review summarizes differences in cardiovascular risk factors and disparities in management and outcomes of ischemic heart disease, heart failure, aortic stenosis, and atrial fibrillation. It also provides an overview of female representation as participants and leaders of clinical trials, editorial boards, and academic institutions. Strategies to overcome these disparities are proposed with examples of successful programs.

Gender-related differences in electrocardiographic parameters and their association with cardiac events in patients after myocardial infarction.

There are limited data regarding gender-related differences in electrocardiographic (ECG) presentation in patients after myocardial infarction (MI) and the prognostic value of ECG variables in women. A series of ECG parameters were analyzed in 838 patients (216 women, 622 men) using standard electrocardiography performed 5 to 7 days after first MI, and their associations with gender and risk for cardiac events, defined as cardiac death, nonfatal MI, or unstable angina, were evaluated. Heart rate was faster and QTc duration was longer, whereas QRS duration was shorter in women compared with men. Women had more lateral ST depressions and more T-wave inversions in the anterior and lateral regions. During mean 2-year follow-up, there were 138 events in men and 65 in women; women had a 38% greater risk for recurrent events (adjusted hazard ratio [HR] 1.38, p = 0.031). In multivariate Cox regression analysis, ST-segment elevation in leads V(1) to V(4) on the fifth to seventh day after MI was associated with increased risk for recurrent events in women (adjusted HR 2.16, p = 0.003) but not in men (adjusted HR = 0.81, p = 0.32). ST depressions in leads V(5), V(6), I, or aVL (adjusted HR 1.70, p = 0.006) in men but not in women (adjusted HR 0.98, p = 0.93) were identified as a risk factor for recurrent events. In conclusion, there are gender-related differences in ECG presentation and the prognostic significance of ECG findings after MI. ST-segment elevation in anterior leads is a significant predictor of events in women, whereas ST depression in lateral leads is a significant predictor in men.

Is obstructive sleep apnea associated with ventricular tachycardia? A retrospective study from the National Inpatient Sample and a literature review on the pathogenesis of Obstructive Sleep Apnea.

BACKGROUND: Obstructive sleep apnea (OSA) is a known independent risk factor for a multiple cardiovascular morbidities and mortality. The association of OSA and ventricular arrhythmias is less well understood. The aim of this analysis is to study the relationship between OSA and ventricular tachyarrhythmias. HYPOTHESIS: OSA is associated with increased ventricular arrhythmias. METHODS: Data from the national inpatient sample (NIS) 2012 to 2014, were reviewed. Discharges associated with OSA were identified as the target population using the relevant ICD-9-CM codes. The primary outcome was a diagnosis of ventricular tachycardia (VT) in the OSA population. Secondary outcomes include the rate of ventricular fibrillation (VF) and cardiac arrest. Multivariable analyses were performed to examine the association of VT with multiple potential confounding clinical variables. RESULTS: Of 18 013 878 health encounters, 943 978 subjects (5.24%) had a diagnosis of OSA. VT and VF were more prevalent among patients with OSA compared to those without a diagnosis of OSA (2.24% vs 1.16%; P < 0.001 and 0.3% vs 0.2%; P < 0.001, respectively). Odds ratio for cardiac arrest in OSA group was not statistically significant (1, 95% confidence interval 0.97-1.02, P < 0.76). In unadjusted analyses, all examined comorbidities were significantly more common in those with OSA, including diabetes mellitus, hypertension, chronic kidney disease, acute coronary syndrome, and heart failure. CONCLUSION: OSA is associated with increased rates of ventricular tachyarrhythmia.

Pioglitazone inhibits platelet function and potentiates the effects of aspirin: a prospective observation study.

BACKGROUND: Thiazolidinediones (TZDs) are agonists of PPARγ and exert beneficial metabolic effects in patients with diabetes. They may also affect platelet function. OBJECTIVES: To characterize potential platelet inhibitory effect of pioglitazone alone and in the presence of aspirin. METHODS: 20 normal and 20 diabetic subjects were enrolled in a prospective study. On day 1, a blood sample was obtained at baseline and a second one after ingestion of 30mg of pioglitazone. PRP was prepared and platelet aggregation and release were evaluated using ADP, collagen and arachidonic acid as agonists. Subjects returned at 6-9days later after ingesting a single 81mg dose of aspirin and a third blood sample was obtained. The subjects then again ingested 30mg of pioglitazone and a fourth and final blood sample was obtained. Platelet aggregation and release were measured. PRP was incubated with thrombin to activate platelets, and the serum was separated and assayed for thromboxane B2, TGFß and CD40L RESULTS: Pioglitazone alone did not affect aggregation with arachidonic acid. However, following ingestion of both aspirin and pioglitazone aggregation was significantly decreased compared to aspirin alone (P<0.0001). Pioglitazone also potentiated aspirin-induced inhibition of ATP release using either arachidonic acid or collagen. Following pioglitazone alone, TXB(2) release was 32,719±3,585pg/ml which was significantly reduced compared to baseline (42,075±4,479, P=0.0004). Pioglitazone also potentiated the inhibition of TXB(2) release by aspirin. CONCLUSION: Pioglitazone inhibits platelet function and potentiates the inhibitory effects of aspirin.