Relation of plasma brain natriuretic peptide levels in non-ST-elevation coronary disease and preserved systolic function to number of narrowed coronary arteries.

Elevated plasma brain natriuretic peptide (BNP) levels have been described in patients with acute myocardial infarction and left ventricular dysfunction. The aim of the present study was to evaluate circulating BNP levels in patients with coronary artery disease without ST-segment elevation acute myocardial infarction and preserved systolic function and to evaluate the BNP levels in relation to the number of involved coronary vessels. We studied 88 patients with coronary artery disease: group 1 had stable angina, group 2 had unstable angina (UA), group 3 had non-Q-wave myocardial infarction (NSTEMI), and group 0 consisted of 15 healthy subjects. All recruited subjects underwent angiographic examination and echocardiographic evaluation. No patients had heart failure, previous myocardial infarction, or electrocardiographic ST elevation. A significant increase in BNP levels was observed in the UA and NSTEMI groups compared with the stable angina group (stable angina 31.3 pg/ml, UA 147.3 pg/ml, NSTEMI, 165.8 pg/ml, p <0.01), and no differences were found between the UA and NSTEMI groups. Analysis of BNP in relation to the number of involved vessels showed significantly higher BNP levels in patients with 3- than in those with 1- or 2-vessel disease (1 to 45.2, 2 to 127.3, and 3 to 220.8 pg/ml, respectively, p <0.05 and p <0.0001, 3 vs 1- and 2-vessel disease, p = 0.01, respectively). Patients with left anterior descending stenosis had higher BNP levels than those with stenosis in other areas (150.8 vs 52.2 pg/ml, p <0.01). In conclusion, circulating BNP levels appeared elevated in patients with acute coronary syndromes with diffuse coronary involvement, even in the absence of systolic dysfunction or heart failure. BNP was also associated with multivessel disease and left anterior descending involvement.

Brain natriuretic peptide levels during cardiac reperfusion: comparison between percutaneous coronary angioplasty and aorto-coronaric bypass.

BACKGROUND: Several studies have documented brain natriuretic peptide (BNP) behavior during cardiac ischemia and after myocardial necrosis. Peptide levels have been shown to be increased during acute phase of cardiac ischemia and during late ventricular remodelling; however, there are fewer data about hormone levels during percutaneous transluminal coronary angioplasty (PTCA) and aorto-coronaric by pass (CABG). METHODS: Aim of this study was to investigate plasma BNP during acute or sub-acute myocardial ischemia in patients undergoing to PTCA or CABG, taking blood samples before and after both procedures. We studied 59 consecutive subjects, 25 submitted to coronary by-pass and 34 submitted to coronary angioplasty. Blood BNP levels were measured the day before intervention and after 3, 7 and 90 days from the procedures. RESULTS: Peptide levels were significantly different just before intervention (GABG group 118.7+/-81 pg/ml vs. PTCA group 34.8+/-15 pg/ml, p<0.01). This difference was increased after 3 days (CABG group 403.2+/-185 pg/ml vs. PTCA group 105.3+/-56 pg/ml, p<0.0001) and after 7 days (CABG group 252.2+/-93 pg/ml vs. PTCA group 69.8+/-36 pg/ml, p<0.00001). These results trend to converge after 90 days (CABG group +/-93 pg/ml vs. PTCA group +/-36 pg/ml, p<0.05). CONCLUSIONS: Plasma BNP shows a different behavior during and after different myocardial reperfusion procedures. PTCA causes only mild and temporary elevation of peptide levels, otherwise CABG demonstrates a more enhancing of BNP release not only in early phase but also after one week; increased levels tend to return towards the reference range after few weeks from cardiac surgery.

Left ventricular diastolic function improvement by carvedilol therapy in advanced heart failure.

Carvedilol treatment in chronic heart failure (CHF) patients has been demonstrated to reduce mortality by improving cardiac systolic function and reducing left ventricular adverse remodeling. However, the effects of the drug on left ventricular (LV) filling are less studied. In this study we evaluated early and long-term diastolic cardiac modifications by an echo-Doppler method during carvedilol therapy in patients with advanced CHF and pseudonormal or restrictive filling pattern. We studied 58 patients with severe but stable CHF (39 in class NYHA III and 19 in IV) having systolic and diastolic dysfunction caused by idiopathic or ischemic cardiomyopathy. Thirty-two patients were randomized to receive previous treatment plus carvedilol (group 1) and 26 continued standard therapy (group 2). In all subjects we evaluated LV volumes, LV mass, LV ejection fraction (EF), and the following transmitral filling parameters: early wave (E), atrial wave (A), E/A ratio, deceleration time (DT), and isovolumetric releasing time (IVRT). After 4 months of therapy, the carvedilol group showed a significant increase of A wave (P < 0.001), DT (P < 0.0001), IVRT (P < 0.0001), and a significant reduction of E/A ratio (P < 0.0005) with respect to group 2. Further improvement was observed at 12 months (A P < 0.0005; DT P < 0.00002; IVRT P < 0.000004; E/A P < 0.0008), although an E wave reduction was observed in group 1 with respect to controls (P < 0.001). Moreover, after 1 year of follow-up a reduction of systolic volume (P < 0.001) and pulmonary pressure (P < 0.0001) and consequent increase of EF (P < 0.001) was observed in the carvedilol group. Carvedilol treatment improved diastolic function in CHF with severe diastolic and systolic impairment at early time, converting a restrictive or pseudonormal filling pattern into an altered pattern. These changes remained significant after 1 year of therapy together with improvement in systolic function.