PV belongs to an established autoimmune disease cluster that includes AITD, rheumatoid arthritis and type 1 diabetes. Our data suggest the possibility of common genetic elements across clinically distinct diseases that might underlie autoimmune susceptibility.

There was an increased prevalence of intra-LV dyssynchrony in obese subjects, especially longitudinal and radial dyssynchrony. This dyssynchrony may signal a mechanism by which obesity predisposes to the development of heart failure.

The benefits of aldosterone receptor antagonists (spironolactone and eplerenone) for patients with heart failure were shown in 2 recent randomized controlled trials. Some of the proposed mechanisms of action of aldosterone antagonists are (1) inhibition of myocardial and vascular remodeling, (2) blood pressure reduction, (3) decreased collagen deposition, (4) decreased myocardial stiffness, (5) prevention of hypokalemia and arrhythmia, (6) modulation of nitric oxide synthesis, and (7) immunomodulation. Like many hormone receptors, the aldosterone receptor can be either nuclear or membrane bound. Most of the activities of the aldosterone receptor are subserved by the nuclear receptors and often lead to alterations in gene transcription. Although these agents are well tolerated in carefully selected patient populations that meet the inclusion criteria of large clinical trials, their use in unselected elderly patients with heart failure and multiple comorbidities has been associated with a significant risk of hyperkalemia and renal failure. Although no convincing data exist to predict which individual patients will respond to aldosterone inhibition, patients with more severe heart failure and those with acute myocardial infarction with concomitant heart failure or left ventricular dysfunction are most likely to respond. Theoretically, aldosterone receptor antagonists may also be beneficial in patients with more mild to moderate systolic heart failure or even in those with diastolic heart failure, although direct evidence is still lacking.

We describe a 62-year-old man with a history of multiple myeloma and prostate cancer, presenting with rhabdomyolysis (from a prolonged fall at home), serum calcium 14 mg/dL, and electrocarAddress for reprints: Figure 1. Electrocardiograms at serum calcium levels of: A) 14.0 mg/dl, B) 9.7 mg/dl, and C) 8.8 mg/dl. diogram (ECG) showing coved ST segment elevations in leads V1-V3 typical of Type 1 Brugada syndrome. Hypercalcemia has been reported as a cause of ST elevation mimicking Brugada syndrome. 1-3 There was no family history of sudden death. Potassium was 4.4 meq/L. Echocardiogram showed normal ventricular function. Minimal troponin-I elevation (0.2 mg/dL) was attributed to massive creatine kinase elevation from rhabdomyolysis. ECG changes resolved with hypercalcemia correction (Figure 1). On repeat visits, the patient had unremarkable ECGs. References 1. Littmann L, Taylor L, Brearley, W. ST-segment elevation: A common finding in severe hypercalcemia.

Studies have shown very good correlation between Doppler-derived gradients and gradients obtained by cardiac catheterization (cath) in aortic stenosis (AS). However, the phenomenon of pressure recovery may lead to significant overestimation of aortic valve (AV) gradients by Doppler echocardiography (echo). We hypothesized that echo-derived gradients will be higher in mild-moderate AS because of pressure recovery. We studied 94 patients who had echo and cardiac caths in a span of 1 week. The mean age was 72 +/- 13 years, 54% males, 79% had coronary artery disease, and the mean left ventricular ejection fraction was 45 +/- 22%. The mean cardiac output and cardiac indices were 5.1 +/- 1.4/2.7 +/- 0.6 (l/mt), (l/m(2)), respectively. For those with mild AS, echo overestimated gradients in 9.5% of patients (4/42) by an average of 19 mmHg, thus misclassifying the degree of stenosis. In those with moderate AS, 14% (3/21) were misclassified as severe AS (gradient overestimation by an average of 13.6 mmHg). In those with severe AS, echo underestimated gradients in 13% (4/31) by an average of 22.7 mmHg. The aorta at the sinotubular junction was 2.8 cm in those patients with mild AS in whom gradients were overestimated by more than 20 mmHg compared to a sinotubular junction diameter of 3.12 cm in those with mild AS and no overestimation of gradients. The AV area/aortic root ratio was 0.4 in those with mild AS and 0.2 in those with severe AS (P < 0.05).