Prognostic effects of calcium channel blockers on cardiac events, stroke and end-stage renal disease in patients with angina pectoris. Retrospective comparative study of benidipine, diltiazem and nifedipine.

BACKGROUND AND AIM: Calcium channel blockers (CCBs) have been reported to reduce the incidence of stroke in hypertensive patients. CCBs are also commonly used to treat patients with angina pectoris (AP). However, there are very few reports on their effects on cardiovascular events, including stroke and end-stage renal disease (ESRD), in patients with AP. This study was designed to assess the differences among CCBs regarding the occurrence of cardiovascular events in patients with AP. METHODS: Clinical records of 226 patients with AP who had received treatment with CCBs in hospital from January 1, 1993 to December 31, 2006 were reviwed. The influence of patient characteristics and medication on the occurrence of cardiovascular events was evaluated (median follow-up period: 4.4 years). Of these 226 patients, 155 were treated with benldipine (CAS 91599-74-5), 36 with diltiazem (CAS 33286-22-5), and 35 were treated with nifedipine (CAS 21629-25-4). RESULTS: Cox proportional hazard regression analysis showed that benidipine was the only CCB that significantly reduced the occurrence of cardiovascular events (HR = 0.39, p < 0.05). Benidipine treatment was associated with higher cardiovascular- and cardiac event-free rates than diltiazem treatment, and higher stroke- and ESRD-free rates than nifedipine. CONCLUSION: This study demonstrated that benidipine prevents the occurrence of cardiovascular events in patients with AP, suggesting that benidipine contributes to a favorable long-term prognosis of such patients.

A serious clinical course of a very elderly patient with takotsubo cardiomyopathy.

An 86-year-old woman was admitted to our hospital because of vomiting and anorexia. Although serum cardiac markers, an electrocardiogram, and echocardiography suggested acute myocardial infarction, emergency cardiac catheterization revealed akinesis of the left ventricular apex without significant coronary artery stenosis. She was diagnosed as having takotsubo cardiomyopathy. The left ventricular dysfunction was considered transient and reversible but did not improve at all, contrary to our expectations. She died of worsening heart failure on day 14. We discuss this serious clinical course of a very elderly patient with takotsubo cardiomyopathy.

Ventricular septal perforation in a patient with takotsubo cardiomyopathy.

An 84-year-old woman was admitted with anorexia and because the serum cardiac markers, electrocardiogram and echocardiography suggested acute myocardial infarction she underwent emergency cardiac catheterization. Coronary angiography revealed no significant coronary artery stenosis, but left ventriculography revealed akinesis of the left ventricular apex with shunt flow to the right ventricle. The diagnosis was a rare case of takotsubo cardiomyopathy complicated by ventricular septal perforation. The patient died of cardiogenic shock on the day of admission day.

Catheter interventional therapy in an elderly patient with deep vein thrombosis and a brain tumor.

A 92-year-old woman with a brain tumor developed swelling of the left lower extremity. Venography showed considerable thrombi from the left common iliac vein to the femoral vein. Following implantation of a temporary inferior vena cava filter, catheter aspiration therapy and catheter-directed thrombolysis were performed. Venography after 3 days showed disappearance of the thrombi and an improvement in vein flow. A permanent inferior vena cava filter was implanted. Local intensive thrombectomy and thrombolysis by catheter together with a temporary inferior vena cava filter were effective treatments in this elderly patient with deep vein thrombosis.

Response of the left anterior descending coronary artery to acetylcholine in patients with chest pain and angiographically normal coronary arteries.

Because atherosclerotic plaque burden affects the likelihood of plaque rupture, it is important to determine the presence and extent of atherosclerotic plaque. We hypothesized that endothelial dysfunction becomes more prominent with development of atherosclerotic plaque; therefore, we examined the relation between coronary endothelial dysfunction and the presence of atherosclerotic plaque. In 36 patients with normal coronary arteries, acetylcholine (ACh; 3 and 30 microg/min) and nitroglycerin were infused into the left coronary ostium, and the diameter of the left anterior descending (LAD) coronary artery was quantitatively measured in response to each drug. The plaque burden was measured in the same segment using intravascular ultrasonography. The plaque burden was 31.2 +/- 2.1% and correlated inversely with changes in coronary diameter induced by 3 microg/min of ACh (r = -0.754, p <0.0001), 30 microg/min of ACh (r = -0.552, p = 0.0005), and nitroglycerin (r = -0.531, p = 0.0009). Multivariate regression analysis showed that the change in coronary diameter induced by 3 microg/min of ACh was associated with plaque burden, independent of the effects of nitroglycerin-induced dilation. Receiver-operating characteristics analysis demonstrated that a cut-off value for the change in coronary diameter induced by 3 microg/min of ACh for predicting a plaque burden of >30% was 0%, with a sensitivity of 0.82 and a specificity of 0.95. These findings suggest that coronary endothelial dysfunction is correlated with atherosclerotic plaque burden, indicating that atherosclerotic plaque may be detected based on coronary endothelial function as assessed by low-dose ACh infusion.

Nicorandil-induced preconditioning as evidenced by troponin T measurements after coronary angioplasty in patients with stable angina pectoris.

Nicorandil has been reported to have a preconditioning effect which suppresses the ST-segment shift or lactate production during coronary angioplasty in patients with stable angina pectoris. The present study investigated whether the preconditioning effect of nicorandil affects troponin T (TnT) levels after coronary angioplasty. Twenty-four patients with stable angina pectoris were randomized to receive a 1-minute intravenous infusion of nicorandil (100 microg/kg) or normal saline. Five minutes later they underwent three 2-minute balloon inflations 5 minutes apart. The sum of ST-segment elevation in all leads (Sum-ST) was determined at the end of each balloon inflation. Serum levels of TnT were measured 6 and 18 hours after the procedure, and the higher value of the two measurements was compared between the groups. SumST decreased progressively during the three sequential balloon inflations in both groups and was less in the nicorandil group than in the control group. The TnT level after the procedure was significantly lower in the nicorandil group than in the control group (0.05+/-0.05 vs 0.11+/-0.10 ng/mL). In conclusion, pretreatment with intravenous nicorandil suppresses TnT release after coronary angioplasty as well as ST-segment elevation during coronary angioplasty, suggesting pharmacological preconditioning by nicorandil.

Preconditioning effect during coronary angioplasty in patients with stable angina pectoris.

OBJECTIVE: To determine whether collateral recruitment is involved in the preconditioning effect on the electrocardiogram, chest symptoms, and lactate metabolism during coronary angioplasty in patients with stable angina pectoris. METHODS AND PATIENTS: Sixteen patients with stable angina pectoris underwent three consecutive 2-min balloon inflations 5-min apart. The greatest ST elevation (deltaSTmax), the sum of ST elevations in all leads (sum(ST)), and QT dispersion (QTd) were measured at the end of each balloon inflation. Chest pain score was evaluated on a scale ranging from no pain (0) to the most severe pain (10). Lactate extraction ratio (LER) was determined by simultaneous blood sampling from the aorta and the coronary sinus. Collateral flow index (CFI) was derived from simultaneous measurements of mean aortic pressure and coronary wedge pressure obtained from a pressure guidewire during balloon inflation. RESULTS: Significant decreases were noted in deltaSTmax (3.3+/-2.1 vs. 3.0+/-1.9 vs. 2.6+/-1.8 mm, p<0.01), sum(ST) (9.7+/-7.2 vs. 8.5+/-6.1 vs. 6.9+/-5.3 mm, p<0.01), QTd (55.3+/-13.8 vs. 46.9+/-9.0 vs. 42.5+/-10.0 ms, p<0.01), and chest pain score (4.3+/-3.1 vs. 2.8+/-2.6 vs. 1.4+/-1.5, p<0.01) during the three sequential balloon inflations. LER significantly increased (-55.5+/-47.8 vs. -36.7+/-34.3 vs. -19.6+/-26.2%, p<0.01), indicating decreased lactate production. No significant difference was observed in CFI (0.16+/-0.10 vs. 0.15+/-0.10 vs. 0.15+/-0.10). CONCLUSION: Repeated balloon inflations during coronary angioplasty elicited a preconditioning effect on ST-segment shift, QT dispersion, chest pain, and lactate production that does not involve collateral recruitment.

Nicorandil enhances myocardial tolerance to ischemia without progressive collateral recruitment during coronary angioplasty.

Nicorandil, a hybrid nitrate and ATP-sensitive potassium channel opener, has had a preconditioning effect in some coronary angioplasty studies. The present study investigated whether the cardioprotective effects of nicorandil involve coronary collateral function. Thirty-two patients with stable angina pectoris were randomized to receive a 1-min intravenous infusion of nicorandil (100 microg/kg) or normal saline. Five minutes later they underwent three 2-min balloon inflations 5-min apart. The maximum ST-segment elevation (deltaSTmax), the sum of ST-segment elevations in all leads (sigmaST), and the chest pain score were determined at the end of each balloon inflation. The collateral flow index (CFI) was derived from simultaneous measurement of the mean aortic pressure and the coronary wedge pressure obtained from a pressure guidewire during balloon inflation. The deltaSTmax, sigmaST, and chest pain score decreased progressively during the 3 sequential balloon inflations in both groups, and the deltaSTmax and sigmaST were less in the nicorandil group than in the control group during each inflation. The CFI did not change during the 3 inflations in either group and was similar in the 2 groups during each inflation. In conclusion, pretreatment with intravenous nicorandil enhances myocardial tolerance to ischemia without progressive collateral recruitment during coronary angioplasty.