Obesity is associated with a wide variety of electrocardiographic (ECG) abnormalities. Most of these reflect alterations in cardiac morphology. Some serve as markers of risk for sudden death. Key ECG abnormalities or alterations occurring with disproportionately high frequency in obese subjects include: leftward shifts of the P wave QRS and T wave axes, various changes in P wave morphology, low QRS voltage, various markers of left ventricular hypertrophy (particularly the Cornell voltage and product), T wave flattening in the inferior and lateral leads, lengthening of the corrected QT interval and prolonged QT interval duration. Alterations in the signal-averaged ECG and in heart rate variability may be arrhythmogenic. Cardiac arrhythmias have been described in obese subjects, but are often accompanied by left ventricular hypertrophy or the sleep apnea syndrome. Many of these ECG abnormalities are reversible with substantial weight loss. Thus, obesity is associated with a wide variety of ECG abnormalities, many of which are corrected by weight loss.

BACKGROUND Guidelines recommend nonstatin lipid-lowering agents in patients at very high risk for major adverse cardiovascular events (MACE) if low-density lipoprotein cholesterol (LDL-C) remains ≥70 mg/dL on maximum tolerated statin treatment. It is uncertain if this approach benefits patients with LDL-C near 70 mg/dL. Lipoprotein(a) levels may influence residual risk. OBJECTIVES In a post hoc analysis of the ODYSSEY Outcomes (Evaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With Alirocumab) trial, the authors evaluated the benefit of adding the proprotein subtilisin/kexin type 9 inhibitor alirocumab to optimized statin treatment in patients with LDL-C levels near 70 mg/dL. Effects were evaluated according to concurrent lipoprotein(a) levels. METHODS ODYSSEY Outcomes compared alirocumab with placebo in 18,924 patients with recent acute coronary syndromes receiving optimized statin treatment. In 4,351 patients (23.0%), screening or randomization LDL-C was <70 mg/dL (median 69.4 mg/dL; interquartile range: 64.3–74.0 mg/dL); in 14,573 patients (77.0%), both determinations were ≥70 mg/dL (median 94.0 mg/dL; interquartile range: 83.2–111.0 mg/dL). RESULTS In the lower LDL-C subgroup, MACE rates were 4.2 and 3.1 per 100 patient-years among placebo-treated patients with baseline lipoprotein(a) greater than or less than or equal to the median (13.7 mg/dL). Corresponding adjusted treatment hazard ratios were 0.68 (95% confidence interval [Cl]: 0.52–0.90) and 1.11 (95% Cl: 0.83–1.49), with treatment-lipoprotein(a) interaction on MACE ( P interaction = 0.017). In the higher LDL-C subgroup, MACE rates were 4.7 and 3.8 per 100 patient-years among placebo-treated patients with lipoprotein(a) >13.7 mg/dL or ≤13.7 mg/dL; corresponding adjusted treatment hazard ratios were 0.82 (95% Cl: 0.72–0.92) and 0.89 (95% Cl: 0.75–1.06), with P interaction = 0.43. CONCLUSIONS In patients with recent acute coronary syndromes and LDL-C near 70 mg/dL on optimized statin therapy, proprotein subtilisin/kexin type 9 inhibition provides incremental clinical benefit only when lipoprotein(a) concentration is at least mildly elevated. (ODYSSEY Outcomes: Evaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With Alirocumab; NCT01663402 )

Cardiovascular disease is a leading cause of morbidity and mortality in chronic hemodialysis patients. Most patients with chronic kidney disease have hypertension and its prevalence remains high following renal replacement therapy. Early studies suggested that hypertension was a risk factor for total and cardiovascular mortality in chronic hemodialysis patients, but the results of more recent studies have caused experts to question these assertions. Systolic hypertension, widened pulse pressure, and nondipping may be better predictors of mortality compared to diastolic hypertension or increased mean arterial pressure. Hypertension in hemodialysis patients is a risk factor for left ventricular hypertrophy (LVH), diastolic dysfunction, and congestive heart failure; good blood pressure control may promote its regression. Atherosclerosis and ventricular arrhythmias may also be linked to hypertension. Thus blood pressure control with a focus on systolic pressure appears to be a prudent strategy to improve cardiovascular outcomes in hemodialysis patients.