Endothelial dysfunction in heart failure identifies responders to cardiac resynchronization therapy.

BACKGROUND: The presence of endothelial dysfunction is associated with increased heart failure mortality. Cardiac resynchronization therapy (CRT) improves heart failure outcomes; however, current guidelines do not adequately identify responders to CRT. OBJECTIVE: The purpose of this study was to determine whether endothelial dysfunction can predict response to CRT. METHODS: Brachial artery flow-mediated dilation, a measure of endothelial function, was measured at baseline preimplant and 90 days postimplant in 33 patients undergoing CRT (age 64.2 +/- 16.8 years, left ventricular ejection fraction [LVEF] 25% +/- 9%, QRS duration 158 +/- 25 ms, New York Heart Association class III-IV). RESULTS: Of the 33 patients, 19 (58%) were responders to CRT. Baseline flow-mediated dilation was 4.6% +/- 4.5% in responders and 8.6% +/- 4.2% in nonresponders (P <.01). After 90 days of CRT, responders had significant improvement in LVEF (23% +/- 8% to 30% +/- 9%, P = .03), 6-minute walk distance (756 +/- 213 feet to 1,089 +/- 242 feet, P = .04), and quality of life (52 +/- 22 to 31 +/- 28, P <.005), whereas nonresponders did not show improvement in these measures. The presence of baseline endothelial dysfunction correlated with impaired baseline functional capacity (r = 0.39, P = .03), and improvement in flow-mediated dilation correlated with improvement in 6-minute walk distance (r = 0.34, P = .05). Logistic regression analysis showed that every 1% reduction in baseline flow-mediated dilation correlated with an approximately 5% increased likelihood of response to CRT. The predictive value of baseline endothelial dysfunction was independent of QRS duration, LVEF, or dyssynchrony and provided additive prognostic value. CONCLUSION: The presence of endothelial dysfunction independently identifies CRT responders and provides additive prognostic value for predicting response over current criteria. Addition of endothelial function assessment to current selection criteria may improve the ability to identify CRT responders.

Statin pretreatment is protective despite an association with greater coronary artery disease burden in patients presenting with a first ST-elevation myocardial infarction.

The relationship of chronic pre-event statin use with coronary disease severity at the time of presentation with a first acute ST-elevation myocardial infarction (STEMI) is unknown. A retrospective review was performed of consecutive patients presenting with STEMI and without a prior history of vascular disease, divided into those whom had been treated with statins before presentation (n=50) and those whom were not pretreated (n=231). Patients pretreated with statins were more likely to have left main (24.0% vs 8.3%; P=.001) or 3-vessel disease (44.0% vs 25.1%; P=.007) vs untreated patients. After matching for risk factors, a trend toward higher likelihood of 3-vessel disease persisted in the statin pretreatment group (47.6% vs 28.6%; P=.07). Significantly lower peak troponin-I levels (87.8 mg/dL vs 134.5 mg/dL; P=.006) were found in patients pretreated with statins, suggesting that statin pretreatment is protective in patients with STEMI despite the presence of greater disease burden. This finding supports the concept that statin therapy alters the natural history of coronary artery disease development leading to a first STEMI and is cardioprotective in those patients who experience a first STEMI.