Prognostic value of serum parathyroid hormone level in acute decompensated heart failure.

BACKGROUND: Secondary hyperparathyroidism develops as a compensatory response to chronic heart failure (HF) and renal failure. The role of parathyroid hormone (PTH) level in acute decompensated HF remains unclear. The aim of this study was therefore to investigate the relationships among mortality, renal function, and serum PTH level in acute decompensated HF patients. METHODS AND RESULTS: A total of 266 consecutive patients admitted for acute decompensated HF without acute coronary syndrome (78±12 years; 48% male) were enrolled. Demographic, clinical, and laboratory characteristics were obtained on admission.During 1-year follow-up, 65 patients (24%) died. Serum PTH level on admission was within the normal range (10-65 pg/ml) in 108 patients (41%), of whom 39 (15%) had low-normal PTH (10-40 pg/ml). On Kaplan-Meier analysis all-cause mortality was significantly higher in patients with low-normal PTH than in those with high-normal (40-65 pg/ml) or high (>65 pg/ml) PTH (log-rank test). On univariate and multivariate Cox regression analysis, low-normal PTH was significantly associated with increased all-cause mortality (unadjusted HR, 2.88; 95% CI: 1.69-4.91; P<0.001; adjusted HR, 3.84; 95% CI: 1.54-9.57; P=0.004). CONCLUSIONS: In patients with acute decompensated HF resulting in hospitalization, low-normal PTH on admission is associated with increased all-cause mortality, regardless of renal function.

Intra-aortic balloon pump induced dynamic left ventricular outflow tract obstruction and cardiogenic shock after very late stent thrombosis in the left anterior descending coronary artery.

An 81-year-old woman had undergone percutaneus coronary intervention to mid left anterior descending coronary artery with a drug-eluting stent for effort angina pectoris. Although she had remained asymptomatic for 3 years, she developed cardiogenic shock following acute myocardial infarction due to stent thrombosis. Her condition deteriorated despite successful revascularization and an initiation of intra-aortic balloon pump (IABP). Transthoracic echocardiography examination revealed systolic anterior motion of the anterior mitral leaflet which caused severe left ventricular outflow tract obstruction (LVOTO) and moderate mitral regurgitation. Discontinuation of IABP resulted in immediate and complete recovery from cardiogenic shock and echocardiography revealed no LVOTO. These findings may shed new light on the underlying mechanism responsible for deteriorating LVOTO and yield new insights into the assessment and the treatment of cardiogenic shock with dynamic LVOTO.

Medtronic Hall valve malfunction due to pannus formation in the aortic position with peculiar movement of the leaflet: a case report.

A 63-year-old woman who had undergone aortic valve replacement (AVR) with a 22-mm Medtronic Hall valve in May 1994 was admitted to the authors' hospital in June 2006 with epigastric pain and nausea. She presented with sudden precipitous deterioration of hemodynamics under high-dose catecholamines, but this improved in ca. 10 min. Valve motion was observed with fluoroscopy for a brief period as prosthetic valve dysfunction was suspected. After 10 min, transient insufficiency in closure of the prosthetic valve was revealed. The patient was diagnosed with prosthetic valve malfunction and referred for an urgent operation. At surgery, pannus was identified at the left ventricular aspect of the prosthetic valve in the aortic position, and this directly restricted leaflet movement during the closing phase. The leaflet movement showed no consistent pattern, but normal movement and half-closure occurred regularly to generate a phenomenon in which alternating normal hemodynamics and low-output syndrome was observed. The patient underwent AVR with a 17-mm St. Jude Medical Regent valve, and was discharged without any complications.