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The amount of myocardial salvage after percutaneous coronary intervention (PCI) is reported to be a major determinant of functional recovery in patients with ST-elevation acute myocardial infarction (MI). However, factors related to the amount of myocardial salvage remain unknown. The goal of this study was to investigate the factors related to the amount of myocardial salvage after emergent PCI in patients with ST-elevation acute MI by incorporating pre- and post-treatment indices and adjunctive treatments.Technetium-99m myocardial imaging was performed before, immediately after, and one month after emergent PCI in 161 patients with ST-elevation acute MI, and the defect score was serially evaluated. A good myocardial salvage was defined as/=4 change (before minus immediately after PCI) of the defect score.Good myocardial salvage was observed in 89 patients. Based on nine clinical variables, logistic regression analysis was performed to determine the important variables related to myocardial salvage. Multivariate analysis revealed that earlier time from onset to PCI (chi (2) = 6.55, P = 0.01, odds ratio = 2.78), larger defect score before PCI (chi (2) = 7.29, P = 0.01, odds ratio = 1.13) and administration of nicorandil before PCI (chi (2) = 9.88, P = 0.008, odds ratio = 4.42) were independently associated with good myocardial salvage. Thrombolysis In Myocardial Infarction (TIMI) flow grade2 before PCI (chi (2) = 4.91, P = 0.03, odds ratio = 0.36) and TIMI flow grade/=2 after PCI (chi (2) = 4.82, P = 0.03, odds ratio = 0.31) were independently associated with poor myocardial salvage. In contrast, the number of asynergic segments before PCI, infarct-related artery, adequate collaterals before PCI and stent implantation were not determinants of myocardial salvage.This study demonstrated that patients with a greater improvement of (99m)Tc tetrofosmin myocardial uptake immediately after PCI had better recovery of left ventricular function and smaller final infarct size. Reperfusion time and TIMI flow grade/=2 after PCI were important determinants of myocardial salvage, and nicorandil was a major determinant of myocardial salvage.

The purpose of this study was to investigate the effects of candesartan on arterial baroreflex sensitivity (BRS) and sympathetic activity in patients with mild heart failure (HF). Arterial pressure, heart rate, plasma renin activity, plasma angiotensin II and noradrenaline, and muscle sympathetic nerve activity (MSNA) were measured before therapy and after 4 weeks in 20 patients with mild HF. Patients were assigned to a candesartan group (n = 10) or a placebo group (n = 10). Baroreflex sensitivity was assessed by using phenylephrine. Candesartan induced an increase in plasma renin activity and plasma angiotensin II associated with a reduction in arterial pressure without affecting heart rate. Although plasma noradrenaline was unchanged (320 +/- 322 pg/ml to 339 +/- 104 pg/ml), MSNA decreased significantly (52 +/- 11 bursts/min to 42 +/- 9 bursts/min; p < 0.01)) and BRS increased significantly (6.9 +/- 3.6 msec/mm Hg to 10.2 +/- 3.3 msec/mm Hg; p < 0.01) after candesartan. However, there were no significant changes in the measured variables in the placebo group. These data indicate that candesartan treatment enhanced BRS and reduced sympathetic activity in patients with mild HF. Thus, the inhibitory effect of candesartan on sympathetic activity may, at least in part, contribute to the beneficial effect of angiotensin II receptor blockade in patients with mild HF.

Although some atypical types of transient left ventricular apical ballooning syndrome have been reported, only a few atypical types of transient mid-ventricular ballooning have been reported. A 70-year-old female underwent surgery for urothelial carcinoma. At day 5 after the surgery, she was admitted to our department without cardiac symptoms because of ST elevation in leads I, II, III, aVF and V1–V6 indicating acute coronary syndrome. She was diagnosed with stress induced cardiomyopathy based on an angiographically normal coronary artery, newly developed extensive wall motion abnormality (hyperbasal contraction and akinesis from the mid-left ventricle to the apex without hypercontraction of the small area adjacent to the apex) based on left ventriculography, and a small elevation of myocardial enzymes incongruous with the area of contraction abnormality. Myocardial scintigraphy with 99m Tc-tetrofosmin showed a severely reduced myocardial perfusion in an extensive mid-ventricular area without a left ventricular base and top of apex, in accord with a wall motion abnormality different from typical apical ballooning or typical mid-ventricular ballooning previously diagnosed in our hospital. This is the first report presenting an atypical mid-ventricular ballooning based on the myocardial atypical perfusion findings.

SummaryA 73-year-old female patient with a past history of right ventricular infundibular stenosis was admitted to our intensive care unit because of right ventricular dysfunction. On the fifth day of hospitalization, she suddenly experienced dyspnea without chest pain despite the improvement of her condition by initial medical treatment. Although electrocardiography revealed no ST-segment elevation, echocardiography and myocardial perfusion using 99mTc-MIBI revealed new development of severe symmetrical akinesia and reduced perfusion of the left ventricular (LV) apex and mid-ventricle. LV apical ballooning syndrome was diagnosed based on the minimal elevation of cardiac enzymes (peak cardiac troponin I 0.18ng/ml) despite the presence of large regions of focal myocardial damage in the myocardium and the absence of positive ECG diagnosis and urgent coronary angiography. Previous coronary angiography revealed normal coronary arteries and the left anterior descending artery without full irrigation around the apex making apical ballooning. On the 12th day of hospitalization, despite the use of positive inotropic treatment, it was impossible to maintain hemodynamic stability, and the patient died prior to the functional recovery of the left ventricle.

A method for exactly solving the condition of contact of the cam and roller follower and analyzing the output displacement of plate cam mechanisms is presented, which have a certain error of the cam profile or a devitation of any kinematic constant from the theoretical value. By using this method, the sensitivities of the output displacement, velocity and acceleration can be evaluated as the ratios of the differences between their actual and ideal values to the deviations of the kinematic constants. Moreover, the relationship between the input angle and the output displacement of the plate cam mechanism with the translating roller follower is precisely measured and the cause for the error of the output displacement is investigated by means of sensitivity curves.

At present, there is no curative strategy for advanced cardiomyopathy except for cardiac transplantation, which is not easily performed, mainly due to a shortage of donors. It has been reported that myocardial progenitor cells exist even in the postnatal heart, suggesting that myocardial progenitor cells could proliferate under some situations and might improve cardiac function in cardiomyopathy-induced hearts. In this study, recombinant human hepatocyte growth factor (rhHGF) was delivered using ultrasound-mediated destruction of microbubbles (UMDM) into the cardiomyopathy-induced heart by doxorubicin (20 mg/kg). Intravenous injection of rhHGF (IV-rhHGF) alone or UMDM alone failed to improve the morphology or the function of the cardiomyopathy-induced heart, but (IV-rhHGF + UMDM) treatment significantly improved the heart morphologically and functionally, and repetitive treatments of (IV-rhHGF + UMDM) enhanced the effects. The number of bromodeoxy-uridine-positive cardiomyocytes significantly increased in the (IV-rhHGF + UMDM)–treated hearts compared with the untreated hearts. Moreover, Sca-1+ myocardial progenitor cells express c-Met, a receptor for HGF. These results suggest that (IV-rhHGF + UMDM) treatment could morphologically and functionally improve the heart in the case of doxorubicin-induced cardiomyopathy through the proliferation of the myocardial progenitor cells.

Atresia of coronary sinus (CS) ostium is a rare abnormality and only a few case reports in association with electrophysiological studies. These patients have been reported to have a variety of several arrhythmogenic sources. A 42-year-old man was referred to our hospital for an electrophysiologic study because of recurrent episodes of palpitation. A 6-French decapolar catheter was introduced from the right jugular vein and advanced to the near the CS ostium. But, we could not be advance the catheter into the CS despite several attempts. On coronary angiogram, an anomalous atresia of the CS ostium was discovered. Regular tachycardia was easily induced by an atrial stimulus, we suggested the patient had an atrioventricular reentrant tachycardia. During the tachycardia, the earliest retrograde atrial activation was recorded in the 5–6 o’clock region of the mitral annulus. The ablation catheter was inserted from the right femoral artery to the accessory pathway (AP) of posterior paraseptal area. Radiofrequency energy was delivered to this site, resulting in elimination of the AP. After this application, there was persistent ventriculo-atrial dissociation and led to successful ablation of the AP. We report a rare case of the ablation procedure of posterior paraseptal AP with atresia of the CS ostium.

SummaryObjectiveAngiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) effectively interfere with the sympathetic nerve activity in patients with left ventricular (LV) dysfunction. The aim of this study was to examine the effect of ARBs on sympathetic nerve activity and baroreflex function in patients with LV dysfunction already receiving ACE inhibitors.MethodsTwenty patients with LV dysfunction already treated with ACE inhibitor (enalapril 5mg/day) were randomly divided into two groups: treatment with 10mg/day enalapril (control group) or 5mg/day enalapril plus 80mg/day valsartan (combination group). In both groups, resting muscle sympathetic nerve activity (MSNA; microneurography), arterial baroreflex sensitivity, and cardiopulmonary baroreflex sensitivity were measured at baseline and 4 weeks after the treatment. Arterial baroreflexes were perturbed by phenylephrine method, and cardiopulmonary baroreflexes were perturbed by lower body negative pressure (−10mmHg).ResultsBaseline characteristics in both groups were similar. Resting MSNA decreased significantly from 35.4±10.8 to 26.4±5.1 burst/min (p