[Multiple percutaneous coronary stent implantation due to myocardial bridging--a case report]. / Wielokrotny zabieg stentowania mostka miesniowego--opis przypadku.

We present a case of a woman who had acute coronary syndrome caused by myocardial bridge. She was treated with percutaneous coronary intervention and stent implantation. Two months after the procedure the patient had myocardial infarction because of subacute thrombosis and during the second intervention another stent was implanted. After a few months another acute coronary syndrome occurred because of restenosis and balloon angioplasty with stent implantation was performed. Despite this the artery occluded and sufficient collateral circulation was developed. Current opinions concerning percutaneous coronary interventions of myocardial bridges are presented.

Fibrosis and cardiac function in obesity: a randomised controlled trial of aldosterone blockade.

OBJECTIVES: As myocardial fibrosis might be an important contributor to the association of obesity with left ventricular (LV) dysfunction and heart failure, we investigated the effects of spironolactone on LV function and serological fibrosis markers (procollagen type III N-terminal propeptide (PIIINP) and procollagen type I C-terminal propeptide (PICP)) in patients with obesity and abnormal LV performance. DESIGN: A prospective, randomised, double-blind, placebo-controlled study. SETTING: A university hospital. PATIENTS AND INTERVENTION: 113 patients (mean±SD age 58±8 years) with body mass index≥30, without any comorbidities, with impaired early diastolic mitral annular velocity, randomised to spironolactone 25 mg/day or placebo for 6 months. MAIN OUTCOME MEASURES: Echocardiographically derived indices of LV systolic (strain and strain rate) and diastolic (E velocity, tissue e' and E/e' ratio) function, myocardial reflectivity (calibrated integrated backscatter (IB)), and serum PICP and PIIINP. RESULTS: In the spironolactone group, significant improvements in myocardial deformation, peak early diastolic velocity (Em), E/e' and IB were noted with a simultaneous decrease in PICP and PIIINP. No corresponding alterations were found with placebo. Improvement in LV systolic function (increase in strain) was independently associated with baseline strain (ß=-0.43, p<0.001), change in IB (ß=0.26, p<0.02) and baseline PICP (ß=0.24, p<0.04). Among the independent determinants of LV diastolic improvement were for increase in Em - baseline Em (ß=-0.44, p<0.001) and baseline PICP (ß=0.35, p<0.002), and for decrease in E/e' - baseline E/e' (ß=-0.35, p<0.005) and change in PICP (ß=0.25, p<0.04). CONCLUSIONS: In patients with obesity without other comorbidities, aldosterone antagonism improves LV function and myocardial acoustic properties, and reduces circulating procollagen levels. Beneficial changes in cardiac performance are independently predicted by baseline LV dysfunction and baseline disturbances, as well as treatment-induced improvements in fibrosis markers. CLINICAL TRIAL REGISTRATION: http://www.anzctr.org.au ACTRN12609000655246.

A randomized study of the beneficial effects of aldosterone antagonism on LV function, structure, and fibrosis markers in metabolic syndrome.

OBJECTIVES: The purpose of this study was to identify the effects of spironolactone on left ventricular (LV) structure and function, and serological fibrosis markers in patients with metabolic syndrome (MS) taking angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. BACKGROUND: Myocardial fibrosis may be an important contributor to myocardial impairment in MS, and aldosterone antagonism may reduce fibrosis. METHODS: Eighty patients (age 59 ± 11 years) with MS, already being treated with angiotensin II inhibition, were randomized to spironolactone 25 mg/day or placebo for 6 months. Each patient underwent baseline and follow-up conventional echocardiography and color tissue Doppler imaging. Raw data files were used to measure calibrated integrated backscatter and to calculate radial and longitudinal strain. Blood was obtained at baseline and follow-up to measure fibrosis markers (procollagen type III amino-terminal propeptide and procollagen type I carboxy-terminal propeptide [PICP]). RESULTS: The spironolactone group showed significant improvement of LV function, myocardial reflectivity, and LV hypertrophy, with a parallel decrease in levels of PICP and procollagen type III amino-terminal propeptide. No analogous changes were seen in the placebo group. Baseline strain (ß = 0.47, p < 0.0001), spironolactone therapy (ß = -0.38, p < 0.0001), and change in PICP level (ß = -0.19, p < 0.03) were independently associated with LV systolic function improvement (increase in strain). Correlates of LV diastolic function improvement (increase in early diastolic mitral annular velocity) were baseline early diastolic mitral annular velocity (ß = 0.47, p < 0.0001), spironolactone therapy (ß = -0.21, p < 0.03), change in PICP level (ß = -0.23, p < 0.02), and age (ß = 0.22, p < 0.04). Favorable effects of spironolactone on cardiac function were not demonstrated in patients with less fibrosis (the lower baseline PICP tertile) or preserved function (the upper baseline strain tertile). CONCLUSIONS: Addition of spironolactone to standard angiotensin II inhibition improved myocardial abnormalities and decreased fibrotic markers in MS. The magnitude of benefit on cardiac performance is determined mainly by baseline LV dysfunction and collagen turnover as well its response to intervention.