Acute physical exertion may trigger an acute coronary syndrome. Furthermore, acute physical exercise may influence hemostatic markers in healthy individuals. However, the effect of acute exercise on blood fibrinolysis and coagulation in patients with coronary artery disease (CAD) is still not well understood.
Nineteen untrained patients with angiographically proven CAD (age, 58 ± 9 years, 12 males), and 25 age- and sex-matched controls without CAD (age, 56 ± 6 years, 16 males) underwent a treadmill exercise test. Global fibrinolytic capacity (GFC) and prothrombin fragment 1 + 2 (F 1 + 2) levels were measured before exercise, at peak exercise, and 2 hours after recovery.
There were no differences between the groups with respect to left ventricular ejection fraction, history of hypertension, body mass index, and serum lipids. Before exercise, GFC was significantly lower in patients with CAD when compared with controls (1.40 ± 0.43 versus 3.28 ± 1.19 μg/mL, respectively; P < 0.001). In patients with CAD, F 1 + 2 levels were significantly higher than those of controls (1.15 ± 0.43 versus 0.79 ± 0.10 nmol/L, respectively; P = 0.002). In both study groups, GFC levels increased significantly at peak exercise and decreased to baseline values 2 hours after recovery. At peak exercise, F 1 + 2 levels significantly increased in both study groups. However, while F 1 + 2 levels of controls decreased to baseline values 2 hours after recovery (0.79 ± 0.10 versus 0.80 ± 0.10 nmol/L; P > 0.05), F 1 + 2 levels of patients with CAD were still significantly elevated (1.15 ± 0.43 versus 1.84 ± 0.06 nmol/L; P = 0.002).
Acute exercise increases coagulation and fibrinolysis both in untrained subjects with and without CAD. However, in patients with CAD, the equilibrium between fibrinolysis and coagulation during peak exercise is disturbed in favor of coagulation after recovery.

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The no-reflow phenomenon during percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI) causes impaired myocardial reperfusion. The aim of the present study was to evaluate the impact of thrombectomy on the prevention for no-reflow phenomenon and for LV remodeling. We performed a retrospective study comparing 116 patients treated for AMI with conventional angioplasty and 89 patients treated for AMI with the combination of angioplasty and thrombectomy. We performed manual aspirating thrombectomy using Thrombuster II. Baseline clinical and lesion characteristics were similar in the 2 groups. No-reflow phenomenon was significantly reduced in the thrombectomy group compared to the controls (8% versus 18%, P < 0.05). Maximum group mean CK was not significantly different between the two groups. During 6 months of follow-up, the mean LV ejection fractions of the 2 groups were not significantly different. However, in the cases involving the proximal left anterior descending (LAD) and right coronary arteries, changes in LV end-diastolic volume index (LVEDVI), LV end-systolic volume index, maximum CK and the incidence of LV remodeling, defined as an increase in LVEDVI of > 20%, were significantly lower in the thrombectomy group than in the control group. Multiple logistic regression analysis indicated that thrombectomy with Thrombuster II significantly reduced the no-reflow phenomenon and LV remodeling. These results suggest that adjunctive pretreatment with a manual aspirating thrombectomy by Thrombuster II reduces the no-reflow phenomenon, and in cases involving the LAD and right coronary arteries, protects against LV remodeling in AMI.

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Recently, the use of sirolimus-eluting stents (SES) has been demonstrated to significantly reduce the rate of adverse events among selected patients with ST-segment elevation acute myocardial infarction (STEMI). We present real-world experience from a single center registry evaluating the safety and efficacy of primary percutaneous coronary intervention (PCI) in unselected patients with STEMI using SES. Clinical outcome at 300-day follow-up in two cohorts of 225 consecutive patients who underwent bare metal stent (BMS) (January 2004 - February 2005, n = 123) or SES (March 2005 - December 2006, n = 102) implantation was examined. The primary endpoint was a composite of major adverse cardiovascular events (MACE: death, nonfatal reinfarction, and target vessel revascularization [TVR]). The incidence of short-term MACE was similar between the SES group and BMS group (30-day rate of MACE: 4.9% versus 8.9%, P = 0.30). Angiographically documented stent thrombosis within 30 days after primary PCI was not diagnosed in any patient in the SES group and occurred in 1 patient treated with BMS (0 versus 0.8%, P = 1.0). At 300 days, SES implantation significantly reduced the incidence of MACE (7.8% versus 22.8%, hazard ratio [HR] 0.32 [95% confidence interval (CI) 0.15 to 0.71], P = 0.005), mainly due to a marked reduction in the risk of TVR (1.0% versus 17.1%, HR 0.05 [95% CI 0.01 to 0.39], P < 0.001). There was no new onset of documented stent thrombosis between 30 and 300 days in either group. Thus, this real-world registry confirmed the safety and efficacy of SES with remarkably lower rates of TVR and MACE in the setting of primary PCI for unselected patients with STEMI in a real-world scenario.

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We conducted this study to verify the efficacy of atrial unipolar potentialfor for ablation of atrial tachycardia. The morphology of atrial unipolar potential at the successful and the best unsuccessful ablation sites was analyzed in 35 patients with atrial tachycardia (sino-atrial reentrant tachycardia (SART) 15, adenosine-sensitive atrial reentrant tachycardia near the His bundle (HAT) 10, and non-reentrant ectopic atrial tachycardia (EAT) 10). The usefulness of atrial unipolar potential was compared with the Ao-Po interval. The incidences of QS pattern at the successful and the best unsuccessful sites were (successful versus unsuccessful; P, respectively) 93 versus 55%; P = 0.20 in SART, 90 versus 0%; P = 0.0001 in HAT, and 90 versus 10%; P = 0.001 in EAT. The mean Ao-Po intervals at the successful and the best unsuccessful sites were 35 versus 30 ms; NS in SART, 48 versus 45 ms; NS in HAT, and 58 versus 50 ms; NS in EAT. A significantly higher incidence of transient success at QS pattern sites was observed in SART than in HAT or EAT (n = 2 ± 0.8 versus 0.2 ± 0.1 and 0.1 ± 0.1, P = 0.0005), and each transient site and final success site in SART was distributed linearly. The sensitivity and specificity of QS patterns with regard to the determination of appropriate target sites were 0.91 and 0.45 in SART, 0.9 and 1.0 in HAT, and 0.88 and 0.88 in EAT, respectively. In ablation of HAT and EAT, the QS pattern is very useful and should be given high priority when determining the optimum target site. In SART, the ablation success was often achieved by multiple, linear RF delivery near perinodal tissue, and the QS pattern could be a candidate for the optimum target site.

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Background: The use of DDIR mode has been limited since the advent of mode switch in the DDDR mode. In patients with AV block, DDDR is necessary to maintain AV synchrony. However, DDIR mode may still be beneficial for patients with intact AV conduction. The aim of this study was to compare the incidence of ventricular pacing and atrial tachyarrhythmia in DDIR and DDDR with mode switch in a randomized, single-blind, crossover study, and discuss the utility of both modes.
Methods and results: Twenty-four patients (8 males) with bradycardia-tachycardia syndrome and no signs of AV block (mean age 70.1 ± -9.1 years) were enrolled and randomized to DDIR or DDDR modes with the leads placed at the right atrial appendage and right ventricular apex. After 12 weeks, patients were switched to the opposite mode. During the study period, atrial high rate episodes and other pacemaker diagnostic data were collected. Significantly less ventricular pacing was observed in DDIR mode (DDIR versus DDDR; 48.9%, 76.5%, P = 0.0002) and atrial high rate episodes were significantly lower in DDIR mode (DDIR versus DDDR; 1.32, 1.85 per day, P < 0.05).
Conclusion: In patients with sinus node dysfunction and intact AV conduction, DDIR mode may have important implications for simplifying device programming, device longevity, and to avoid atrial tachyarrhythmia.

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Diabetic patients often have manifestation of coronary heart disease. As a consequence, therapeutic strategies for diabetes should pay more attention to hypoglycemic agents which do not have adverse effects on myocardium. Mitiglinide is considered to have little or no impact on the cardioprotective effect of ischemic preconditioning (IP) because of its high selectivity for blocking sulfonylurea receptor1 (SUR1). However, glibenclamide, a nonselective SUR blocker, attenuates this beneficial effect.
In the present study, we tested the hypothesis that mitiglinide preserves the protective action of IP evaluated by ischemia/reperfusion ventricular tachyarrhythmia (rVT) in isolated perfused rat hearts. After initial perfusion, the hearts were assigned to one of the following groups: 1) non-IP with control perfusion buffer (non-IP group); 2) IP with control perfusion buffer (IP-C group); 3) IP with perfusion buffer containing glibenclamide (IP-G group); and 4) IP with perfusion buffer containing mitiglinide (IP-M group). The protocol for the non-IP group consisted of 21 minutes of aerobic perfusion before 10 minutes of ischemia. In the other 3 groups (IP groups), there were 3 cycles of 2-minute ischemia followed by 5 minutes of reperfusion before 10 minutes of ischemia. The IP-C group had a significantly shorter rVT duration than the non-IP group (4.4 ± 1.8 minutes versus 14.3 ± 2.5 minutes; P < 0.05). rVT duration was the shortest in the IP-M group (3.9 ± 1.0 minutes), but among the longest in the IP-G group (14.0 ± 2.6 minutes).
In conclusion, mitiglinide preserved the cardioprotective effect of IP, however, glibenclamide abolished this beneficial effect. Therefore, mitiglinide may offer a long-term benefit for myocardial ischemia in diabetic patients.

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The electrophysiological effects of carvedilol, a β-blocking agent with vasodilating actions, have been studied on rabbit pacemaker cells using the whole-cell patch clamp technique. Nystatin-perforated patch recordings from the sinoatrial (SA) and atrioventricular (AV) nodes demonstrated that 1-3 μM of carvedilol caused a decrease in the spontaneous firing frequency, depolarization of the maximal diastolic potential, and prolongation of the action potential duration in both species. Voltage clamp experiments were performed using SA and AV node myocytes to identify and define the carvedilol-induced changes in the Ca²⁺ current, I_Ca, delayed rectifier K⁺ current, I_K, and hyperpolarization-activated inward current, I_f. In the SA node cells, 1 μM of carvedilol blocked I_K, I_Ca, and I_f by 72%, 47%, and 22%, respectively. In the AV node cells, the corresponding reductions were 64% (I_K) and 46% (I_Ca), respectively. In both the SA and AV nodes the decrease in I_K appeared to be mainly due to the rapidly activating component of the delayed rectifier, I_Kr, since the high dose of carvedilol blocked I_K in the SA and AV nodes to a submaximal degree. In conclusion, effective doses of carvedilol have classical class III antiarrhythmic actions and a negative chronotropic effect resulting from the inhibition of I_K and I_Ca. Both actions may be efficacious for treating supraventricular tachyarrhythmias. (Int Heart J 2007; 48 : 347-358)

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Mechanical stress by pressure overload due to hypertension or valvular heart disease such as aortic valve stenosis induces cardiac hypertrophy. It has been well established that the mechanical stretch of cardiac myocytes in vitro induces hypertrophic responses such as the expression of immediate early response genes including c-fos. However, it remains uncertain whether the mechanical forces due to pure atmospheric pressure can induce similar responses in cardiac myocytes. We thus cultured rat neonatal cardiac myocytes in an atmospheric pressure chamber apparatus and determined the effects of pure pressure stress on c-fos gene expression. Pressures greater than 80 mmHg enhanced c-fos mRNA after 30 minutes. These results suggest that pure atmospheric pressure overload can also induce early hypertrophic responses in cardiac myocytes.

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Inhibition of matrix metalloproteinases (MMPs) would be expected to suppress atherosclerotic neointimal proliferation and thus limit atheromatous plaque progression, but this has not yet been demonstrated morphologically in atherosclerotic intimal hyperplasia induced by cholesterol loading in experimental animals. We therefore investigated whether a broad-spectrum MMP inhibitor (MMPi), ONO-4817, could inhibit the development of intimal hyperplasia in male hyperlipidemic rabbits (n = 6) fed laboratory chow supplemented with 1% cholesterol for 2 months followed by a 1% cholesterol diet plus 100 mg/kg ONO-4817 for another month (Chol + ONO group). Control animals (n = 6) received no ONO-4817. When the aortas were studied both histologically and immunohistochemically, intimal hyperplasia was inhibited in Chol + ONO rabbits. The distribution of macrophages and MMP-12 in the hyperplastic tissue of the Chol + ONO rabbits was limited to the luminal side of the lesions. No such limitation in the distribution of macrophages and MMP-12 was observed in the control group. The distribution of smooth muscle cells in the hyperplastic tissue was not different between the Chol + ONO and control groups. However, the distribution of MMP-2 and MMP-12 was limited to the luminal side of lesions in the Chol + ONO group. This is the first reported evidence that an MMPi can suppress the development of intimal hyperplasia in hyperlipidemic rabbits.

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A 74-year-old man had undergone on-pump coronary artery bypass grafting (CABG) for effort-induced angina pectoris. Soon after CABG using the left internal thoracic artery for the left anterior descending artery and saphenous vein for the left circumflex artery, ST elevation was found in the inferior leads and complete atrioventricular block, ventricular tachycardia, and circulatory collapse occurred. Emergent coronary angiography revealed diffuse severe spasm of the right coronary artery (RCA). Despite the intravenous and intracoronary administration of massive doses of vasodilators and intra-aortic balloon pumping, the coronary spasm did not resolve. Five stents were deployed from the distal to the proximal portion of the RCA. After multistenting, coronary flow was dramatically improved and the ST elevations in the inferior leads were also improved. Coronary artery spasm after CABG is relatively rare, but when it occurs, it can be fatal. Multistenting is a useful treatment for life-threatening refractory coronary spasm after CABG.

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Coronary embolism is one of the less common causes of acute myocardial infarction (AMI). We describe a 72-year-old man with atrial fibrillation having an AMI, in whom a massive intracoronary thrombus of the right coronary artery was successfully removed by aspiration via a thrombectomy catheter, achieving successful reperfusion with a complete resolution of ST-segment elevation. The appearance of the aspirated material suggested coronary embolism was the cause of the AMI. It is concluded aspiration thrombectomy is a feasible and safe approach for treating coronary embolism.

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Stent thrombosis after sirolimus-eluting stent (SES) implantation has been reported to occur at 6 hours to 26 months after the procedure and usually within 2 weeks after discontinuation of antiplatelet medication.^1-4) However, there are very few reports of stent thrombosis after 2 years. We report 2 cases of very late stent thrombosis after implantation of a sirolimus-eluting stent presenting as acute myocardial infarction (AMI). These late thromboses occurred about 2 years after SES implantation and over 1.5 years after discontinuation of ticlopidine.

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Most tumor invasion into the heart is nonspecific and clinically silent. Myocardium metastasis rarely mimics a myocardial infarction. In this case, a cardiac metastasis from a squamous cell carcinoma presented with both persistent ST elevation and paroxysmal supraventricular tachycardia. The secondary lesion was located in the anterior wall and lateral wall of the left ventricle and induced electrocardiographic changes imitating an acute myocardial infarction.

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Patients with neonatal lupus erythematosus (NLE) often have congenital heart block with or without heart failure and are born to mothers who have anti-SS-A and/or anti-SS-B antibodies. NLE has been considered to result from the placental transmission of maternal autoantibodies into the fetal circulation causing myocardial damage. We report a case of NLE with congenital heart block who had undergone pacemaker implantation at the age of 17, and then developed dilated cardiomyopathy (DCM) at the age of 19, which is much later than in most other cases. The patient's mother was positive for anti-SS-A and anti-SS-B antibodies, whereas the patient was negative for both anti-SS-A and anti-SS-B antibodies. There were some autoantibodies against cell surface antigens of cardiac myocytes in the serum from the patient, and annexin A6 was identified as one of the autoantigens. This is the first report demonstrating that annexin A6 is involved in the myocardial injury in patients with NLE. The results indicate that inhibition of annexin A6 function may prevent autoantibody-mediated myocardial injury in at least some cases of DCM.

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Pulmonary arterial hypertension (PAH) is commonly associated with CREST (Calcinosis, Raynaud phenomenon, Esophageal motility disorders, Sclerodactyly, and Telangiectasia) syndrome. Sildenafil, an oral phosphodiesterase type-5 inhibitor, may offer benefits in the pharmacological management of PAH. However, little is known about the long-term hemodynamic effects of sildenafil, and the potential role of sildenafil in long-term combination with beraprost, an oral prostacyclin analogue, remains unclear. We therefore examined the hemodynamic effect of oral sildenafil alone and when coadministered with beraprost in a patient with PAH associated with CREST syndrome.
Traces of the acute hemodynamic effects of beraprost (20 μg) disappeared after 2 hours. In contrast, the acute hemodynamic effects of sildenafil (50 mg) produced a greater reduction in PAP (31%) and PVR (40%), and these effects also disappeared after 5 hours.
After 1 month of combination therapy of sildenafil (25 mg) twice daily and beraprost (20 μg) 3 times daily, the fall in pulmonary artery pressure and pulmonary vascular resistance was sustained (31% in both). Furthermore, the patient had significantly improved her 3-minute walk test and NYHA function class without significant adverse effects at the reported doses.
The findings indicate that oral sildenafil is a potent pulmonary vasodilator that appears to act synergistically with oral beraprost to cause sustained pulmonary vasodilatation in a patient with PAH associated with CREST syndrome.

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