Preprocedural statin therapy reduces the risk and extent of cardiac biomarker release following percutaneous coronary intervention.

This study evaluates the association between statin therapy in patients treated by percutaneous coronary intervention (PCI) for stable angina pectoris and postinterventional myocardial injury with subsequent long-term clinical outcome. Prospectively collected data on 400 consecutive patients with stable angina pectoris or evidence of inducible myocardial ischemia were analyzed. The incidence of myocardial infarction based on postinterventional release of troponin I>1.5 ng/ml was 12% in the statin pretreated patients and 20% in those not pretreated with statin therapy (P=0.04, odds ratio 1.84, 95% confidence interval 1.06-3.21). Of the patients experiencing a post-PCI troponin elevation>1.5 ng/ml, those pretreated with a statin pre-PCI had a lesser troponin elevation compared with those not receiving a statin pre-PCI (median: 2.9 ng/ml [1.9-11.5] vs 5.0 ng/ml [3.1-8.8]; P<0.001). In the multivariate model, preprocedural statin therapy was identified as the only independent negative predictor of procedure-related myocardial necrosis based on postprocedural troponin elevation. In the 21-month follow-up period, statin pretreated patients were observed to have fewer deaths, revascularizations, or myocardial infarction; however, this difference was not statistically significant. These results suggest that pretreatment with statins in patients undergoing PCI for stable angina pectoris reduces the risk and extent of procedure-related myocardial injury measured by troponin release.

Relationship of C-reactive protein to adverse cardiovascular events in patients treated by percutaneous coronary intervention for stable angina pectoris.

Low-grade inflammation as detected by increased C-reactive protein (CRP) levels predicts the risk of cardiovascular events. However, there is still controversy over the mid-term predictive value of CRP in patients referred for elective percutaneous coronary revascularization (PCI) for stable angina pectoris. The aim of this study was to assess the relationship between baseline CRP level and mid-term outcome of patients undergoing PCI. Two groups of patients with stable angina pectoris were prospectively studied. Group A consisted of 150 consecutive patients with a CRP level < or = 3 mg/L, and group B consisted of 150 consecutive patients with a CRP level > 3 mg/L undergoing PCI at our institution. Comparing both groups of patients, the analysis confirmed a significant difference between medians of the CRP levels (0.5 versus 8 mg/mL; P < 0.001). A higher level of CRP in group B was associated with a lower presence of male gender (P < 0.05) and history of myocardial infarction (P < 0.05). On the other hand, in group B there was higher occurrence of smoking (P < 0.001), hypertension (P < 0.05), hypertriglyceridemia (P < 0.001), and diabetes mellitus (P < 0.01). The incidence of myocardial infarction based on post-interventional release of TnI > 1.5 ng/mL reached 12% in group A and 14% in group B (P = 0.73). Analyses were repeated with adjustment for significant baseline variables, which did not change our findings. The incidence of adverse cardiovascular events during a six month follow-up was 13% in both groups (NS). Increased CRP serum prior to PCI was not associated with the risk and extent of procedure-related myocardial injury measured by TnI release and does not portend heightened cardiovascular risk at six months after percutaneous revascularization. On the other hand, a CRP level > 3 mg/L was associated with a higher occurrence of cardiovascular risk factors (smoking, hypertension, hypertriglyceridemia, and diabetes mellitus).

Effects of alcohol septal ablation for hypertrophic obstructive cardiomyopathy on Doppler Tei index: a midterm follow-up.

Alcohol septal ablation (PTSMA) improves outflow gradient, left ventricular (LV) diastolic function, and symptoms in patients with hypertrophic obstructive cardiomyopathy (HOCM). Tei index (TI) is a Doppler parameter reflecting both systolic and diastolic LV function. Midterm changes of TI after PTSMA have not been determined up to now. Twenty-seven consecutive patients (mean age 53 +/- 13 years) with symptomatic HOCM underwent PTSMA procedure. Clinical and echocardiographic data were collected at baseline, 6 and 12 months after PTSMA. TI decreased from 0.67 +/- 0.11 to 0.55 +/- 0.06, isovolumic contractile time (ICT) decreased from 74 +/- 20 to 48 +/- 11 ms, isovolumic relaxation time decreased from 146 +/- 25 to 117 +/- 9 ms, and LV ejection time decreased from 330 +/- 42 to 298 +/- 13 ms. LV remodeling was determined by LV dimension increase from 46 +/- 6 to 48 +/- 6 mm and basal septum thickness reduction from 22 +/- 4 to 15 +/- 3 mm. LV ejection fraction decreased from 78 +/- 7 to 73 +/- 6% and maximal outflow gradient decreased from 69 +/- 44 to 15 +/- 11 mmHg. All changes were statistically significant (P <0.01). Symptomatic improvement was characterized by relief of dyspnea (2.5 +/- 0.7 versus 1.4 +/- 0.6 NYHA class; P <0.01) and angina pectoris (2.6 +/- 0.9 versus 0.7 +/- 0.7 CCS class; P <0.01). PTSMA is an effective method of therapy for HOCM. Shortening of TI suggests the improvement of LV myocardial performance in the midterm follow-up.

Effects of varying ethanol dosing in percutaneous septal ablation for obstructive hypertrophic cardiomyopathy on early hemodynamic changes.

This prospective, randomized study evaluates the association between ethanol dose and postprocedural hemodynamic changes in 42 patients treated by alcohol septal ablation for obstructive hypertrophic cardiomyopathy. These results suggest that the early course of hemodynamic changes is not related to the use of a small (1 to 2 ml) or standard (>2 ml) dose of ethanol.

Alcohol septal ablation for hypertrophic obstructive cardiomyopathy: Lower alcohol dose reduces size of infarction and has comparable hemodynamic and clinical outcome.

Patients with highly symptomatic hypertrophic obstructive cardiomyopathy (HOCM) are considered to be good candidates for percutaneous transluminal septal myocardial ablation (PTSMA). However, there is ongoing discussion regarding the optimal dose of alcohol injected into target septal artery and the impact of infarct sizes on the clinical and hemodynamic outcome. Thirty-four patients with symptomatic HOCM receiving maximum medical therapy were consecutively enrolled. Patients were randomized in a 1:1 ratio into one of the two arms according to dose of injected alcohol during echocardiography-guided PTSMA procedure. Clinical, electrocardiographic, and echocardiographic evaluation were performed 6 months after the procedure in all the patients. Both groups of patients matched in all clinical and echocardiographic data. The dose of alcohol injected was 1.6 +/- 0.4 and 3.4 +/- 0.9 (P < 0.001) with subsequent peak of CK-MB 1.9 and 3.2 microkat/L (P < 0.05) in group A and B, respectively. There was a correlation between amount of injected alcohol and the peak of CK-MB (r = 0.58; P < 0.01), whereas no significant relationship (r = 0.16; P = NS) was documented between the peak of CK-MB and left ventricular outflow gradient at follow-up. At 6-month follow-up, both groups of patients were not significantly different with regard to symptoms or electrocardiographic and echocardiographic findings. In conclusion, this study suggests that the low dose (1- 2 ml) of alcohol injected into target septal branch reduces size of necrosis. Moreover, the low dose is probably as safe and efficacious as usually used doses (2-4 ml).

The biphasic course of changes of left ventricular outflow gradient after alcohol septal ablation for hypertrophic obstructive cardiomyopathy.

BACKGROUND AND AIM: Alcohol septal ablation (PTSMA) decreases left ventricular outflow gradient (LVOG) and relieves symptoms in patients with hypertrophic obstructive cardiomyopathy (HOCM). The time course of early changes of LVOG has not been clearly determined up to now. METHODS: Doppler echocardiography was used to determine the maximal LVOG. Thirty-nine consecutive patients (24 women; age 55+/-14) were examined at baseline, immediately after the procedure, and 3-5 days, 3 weeks and 3 months thereafter. RESULTS: The baseline LVOG decreased immediately after PTSMA from 73+/-49 mmHg to 13+/-16 mmHg (p<0.01). During the hospital stay (postprocedural period) LVOG increased from 13+/-16 to 37+/-35 mmHg (p<0.01). All the patients were discharged 5-10 days after the procedure. At three-week examination LVOG decreased from 37+/-35 to 25+/-12 mmHg (p<0.01). Three-month survival was 97%. One patient died suddenly one month after PTSMA. At three-month examination LVOG decreased from 25+/-12 to 17+/-14 mmHg (NS). All the patients reported an improvement in symptoms at follow-up. CONCLUSIONS: The immediate decrease of LVOG after PTSMA procedure caused by myocardial necrosis and stunning, was followed by a significant LVOG increase during the early postprocedural period and continuous LVOG decrease at the short-term follow-up.

Relationship of C-reactive protein to presence and severity of coronary atherosclerosis in patients with stable angina pectoris or a pathological exercise test.

BACKGROUND: C-reactive protein (CRP) level is a sensitive marker of inflammation and a probable predictor of cardiovascular risk. The aim of this study was to assess the relationship between the presence and the extent of coronary atherosclerosis and CRP level in patients referred for coronary angiography for stable angina pectoris or a pathological exercise test. PATIENTS AND METHODS: A group of 200 patients were prospectively analyzed for the relationship between the presence and extent of coronary atherosclerosis and high-sensitivity CRP. Patients with stable angina pectoris or a pathological exercise test were included. RESULTS: For the whole group the CRP geometric mean was 2.92 mg/l and the median 3.0 mg/l. There was no difference between groups of patients with different extents of coronary lesions (P = 0.320, one-way analysis of variance). In patients without significant coronary disease the CRP geometric mean was 3.1 (2.28-4.21) mg/l with a variation coefficient of 118.4%; in patients with coronary artery disease the geometric mean was 2.83 (2.34-3.43) mg/l with a variation coefficient of 104.0%. The difference in CRP between both groups was not significant (P = 0.601). There was also no significant difference in CRP levels between groups of patients with and without a history of myocardial infarction (2.65 (2.08-3.36) mg/l and 3.18 (2.54-3.98) mg/l, P = 0.266) respectively. There was no correlation between the classification of angina pectoris and the logarithm of CRP level (P = 0.331). This relationship was not confirmed even in the group of patients with significant coronary artery disease (P = 0.693). CONCLUSIONS: CRP level is not related to the extent or the presence of coronary atherosclerosis assessed by coronary angiography, history of myocardial infarction or class of stable angina pectoris in patients referred for coronary angiography for stable angina pectoris or a pathological exercise test.