Exercise at ventilatory threshold aggravates left ventricular remodeling in patients with extensive anterior acute myocardial infarction.

BACKGROUND: The effects of physical training on ventricular remodeling after extensive anterior acute myocardial infarction (AMI) have not yet been defined. This randomized controlled study examines whether exercise aggravates left ventricular (LV) remodeling in patients with extensive anterior AMI. METHODS: Forty-eight consecutive patients with a first extensive anterior AMI and an LV ejection fraction (EF) of <45% assessed with left ventriculography (LVG) within 3 days of onset were randomly allocated to a training group (n = 24) or a control group (n = 24). Exercise intensity was determined by the heart rate of each patient at ventilatory threshold (VT). Three weeks after onset, a second LVG was performed, followed by a supervised exercise program at VT for 12 weeks. The LVG was reassessed after the exercise program. We then calculated the global LV volume (end-diastolic volume index [EDVI], end-systolic volume index [ESVI]) and systolic expansion volume index (SEVI), a new parameter for measuring the infarction site expansion at the end-systolic phase. RESULTS: Both EDVI and ESVI significantly decreased in the control group from 1 to 4 months after onset (91.2 +/- 26.1 to 83.3 +/- 24.0 mL/m2, P <.05; 52.4 +/- 22.5 to 45.7 +/- 18.8 mL/m2, P <.01, respectively), but not in the exercise group. The SEVI also significantly decreased in the control group from 1 to 4 months (33.1 +/- 16.9 to 25.7 +/- 13.9 mL/m2, P <.05), but not in the training group (34.2 +/- 12.9 to 36.5 +/- 15.5 mL/m2, P = not significant). CONCLUSION: Exercise while healing in patients with extensive anterior AMI, even at the VT level, induces LV enlargement and thus might aggravate LV remodeling. Therefore, in these patients, clinicians should consider withholding exercise training for at least 8 weeks, versus the 3-week period used in this trial.

Effect of atrial septal aneurysm on risk of cerebrovascular events in Japanese patients.

BACKGROUND: The aim of the present study was to determine whether atrial septal aneurysm (ASA) detected by transthoracic echocardiography (TTE) is an independent risk factor of cerebrovascular events for Japanese people. METHODS: A control study was conducted with 178 patients with ASA (follow-up rate, 96.7%; median follow-up period, 5.6 years) and 176 control patients (follow-up rate, 97.8%; median follow-up period, 5.4 years), selected from 42,528 consecutive patients who underwent TTE in the Omiya Medical Center, Jichi Medical School, from April 1991 to March 2001. Data were collected by structured review of patient charts and a subsequent telephone survey. Long-term cerebrovascular risk factors were evaluated by logistic regression analysis. RESULTS: A previous episode of cerebral infarction had occurred in nine ASA patients (5.1%) and 11 control patients (6.3%). During the follow-up period, new cerebral infarction occurred in 12 ASA patients (6.7%) and six control patients (3.4%). Only atrial fibrillation was found to be an independent risk factor of new cerebral infarction (OR, 5.06; 95% CI, 1.32-19.46; P=0.04). CONCLUSIONS: ASA is not an independent risk factor of cerebrovascular events for Japanese patients. Thus, aggressive strategies such as anticoagulation are not essential for ASA patients without embolic episodes.

Recurrent cardiogenic shock caused by dynamic mitral regurgitation in a patient with hypertrophic obstructive cardiomyopathy: a case report.

A 68-year-old man with hypertrophic obstructive cardiomyopathy developed recurrent cardiogenic shock due to dynamic mitral regurgitation. The pressure gradient in the left ventricular outflow tract under medication was 30 mmHg, and he complained of no symptom. He developed shock with dyspnea suddenly after bathing and defecation. Echocardiography and left ventriculography revealed massive mitral regurgitation and mild increment of pressure gradient in the left ventricular outflow tract (50 mmHg). He underwent successful mitral valve replacement following treatment with beta-blocker under intraaortic balloon pumping support. This case illustrates that exacerbation of the systolic anterior motion of the mitral anterior leaflet can cause dynamic severe mitral regurgitation with 'mild' increment of pressure gradient in the left ventricular outflow tract, resulting in cardiogenic shock with severe lung edema.

[Serotonin receptor blockade effective for postprandial vasospastic angina associated with dumping syndrome after esophagectomy: a case report].

A 49-year-old woman was admitted to our hospital because of frequent postprandial esophageal angina. After successful pyloric plasty, chest oppression lasting 5 to 15 min developed postprandially as well as symptoms of dumping syndrome. Electrocardiography showed ST-segment elevation in the II, III, aVf and precordial leads (V2 to V6). Finally, giant positive T waves and U waves were uniquely noted in the V1 to V5 leads. Intracoronary administration of acetylcholine (20 micrograms) provoked severe diffuse spasm in both right and left coronary arteries, chest pain and ST elevation. The conventional treatment for vasospastic angina, such as Ca2+ antagonists, nitrates and K channel opener, achieved no response. However, the combination with serotonergic receptor blockade reduced anginal attack. These findings suggest that the spastic angina in this case was partly caused by serotonin.

[Prospective randomized study of argatroban versus heparin anticoagulation therapy after percutaneous coronary intervention for acute myocardial infarction].

OBJECTIVES: Argatroban, a selective thrombin inhibitor, is expected to decrease acute coronary re-occlusion and restenosis via direct suppression of thrombin generation after percutaneous coronary intervention (PCI) in patients with acute myocardial infarction. This study evaluated the effect of argatroban compared with heparin as an adjunctive anticoagulation therapy after PCI in patients with acute myocardial infarction. METHODS: Fifty-four consecutive patients with acute myocardial infarction underwent PCI within 6 hr from the onset and were randomly allocated to receive argatroban (argatroban group: n = 27) or heparin (heparin group: n = 27) after PCI. Each drug was administered intravenously for 72 hr. Coronary angiography was repeated at 1 and 6 months after the onset of acute myocardial infarction. In-hospital cardiac events, bleeding complications, and long-term outcome were surveyed. RESULTS: Baseline clinical and angiographic variables were similar in the two groups. Acute coronary re-occlusion and major hemorrhagic complications did not occur in either group. Minor bleeding complications, such as hematoma of the puncture sites, occurred significantly less frequently in the argatroban group than in the heparin group (4% vs 30%, p < 0.05). After 6 months, there were no significant differences in restenosis rate and target vessel recanalization rate between the two groups. Subgroup analyses revealed no significant differences in restenosis rate between patients treated with only balloon angioplasty and stent implantation. CONCLUSIONS: Argatroban provides similar prevention of acute thrombotic events and restenosis compared with heparin. However, argatroban might reduce bleeding complications in patients with acute myocardial infarction after PCI.

Rupture of the anterolateral papillary muscle caused by a single diagonal branch obstruction.

This report presents the first case of anterolateral papillary muscle rupture caused by a diagonal branch occlusion only. Although the patient was in shock on admission, he was successfully treated by emergency surgery after hemodynamic stabilization by a percutaneous cardiopulmonary support system. This case implies that the anterolateral papillary muscle has a single blood supply and that it can rupture by an occlusion of only one diagonal branch even after balloon angioplasty.

Exercise training in patients with chronic heart failure improves endothelial function predominantly in the trained extremities.

The present study investigates whether lower-limb dominant exercise training in patients with chronic heart failure (CHF) improves endothelial function primarily in the trained lower extremities or equally in the upper and lower extremities. Twenty-eight patients with CHF were randomized to the exercise or control group. The exercise group underwent cycle ergometer training for 3 months while controls continued an inactive sedentary lifestyle. Exercise capacity (6-min walk test) and flow-mediated vasodilation in the brachial and posterior tibial arteries were evaluated. After 3 months, walking performance increased only in the exercise group (488+/-16 to 501+/-14 m [control]; 497+/-23 to 567+/-39 m [exercise, p<0.05]). The flow-mediated vasodilation in the brachial arteries did not change in either group (4.2+/-0.5 to 4.5+/-0.4% [control]; 4.3+/-0.5 to 4.6+/-0.4% [exercise]), but that in the posterior tibial arteries increased only in the exercise group (4.1+/-0.5 to 4.1+/-0.3% [control]; 3.6+/-0.3 to 6.4+/-0.6% [exercise, p<0.01]). Cycle ergometer training improved flow-mediated vasodilation in the trained lower limbs, but not in the untrained upper limbs. Exercise training appears to correct endothelial dysfunction predominantly by a local effect in the trained extremities.

Effect of reperfusion therapy on cardiac rupture after myocardial infarction in Japanese.

BACKGROUND: Cardiac rupture after acute myocardial infarction (AMI) is unpredictable and almost always fatal, so the present study reviewed all the clinical characteristics of patients with cardiac rupture to determine if its occurrence can be predicted. METHODS AND RESULTS: The clinical characteristics of 1,296 consecutive AMI patients from January 1992 to February 2002 were retrospectively evaluated using multi-logistic analysis. Cardiac rupture occurred in 45 patients (3.5%), comprising left ventricular free wall rupture (n=23), ventricular septal perforation (n=20) and papillary muscle rupture (n=2). Early-phase rupture (within 72 h after AMI onset) was associated with anterior infarction. Of the 45 patients who experienced ruptures, 24 (53.3%) survived to discharge; 21 (46.6%) of the 45 ruptures occurred after admission. Successful reperfusion therapy was performed within 24 h for 840 patients. The incidence of rupture was significantly lower for reperfused patients than for non-reperfused patients (0.6% vs 3.5%, respectively; p<0.01). Peak C-reactive protein concentration was a reliable predictor of late-phase rupture (p=0.01), but not of early-phase rupture. CONCLUSIONS: Reperfusion therapy appears to aid in the prevention of cardiac rupture, especially late-phase rupture.

Effects of a distal protection device during primary stenting in patients with acute anterior myocardial infarction.

BACKGROUND: The angiographic no-reflow phenomenon is an adverse prognostic factor in patients with acute myocardial infarction (AMI). The aim of the present study was to evaluate the effects of an occlusive balloon type distal protection device (PercuSurge GuardWire: GW) during primary stenting in patients with anterior AMI. METHODS AND RESULTS: The GW group included 42 patients treated by primary stenting with GW protection and the control group included 30 patients treated by primary stenting after thrombectomy without distal protection. Left ventricular (LV) function was measured and compared by left ventriculography obtained soon after percutaneous coronary intervention (PCI) and 3 weeks after onset. The corrected TIMI frame count values were lower in the GW group than in the control group (27.5+/-2.3 vs 35.1 +/-2.5, p=0.030). The number of patients with myocardial blush grade 3 after PCI was higher in the GW group than in the control group (45.7 vs 20.0%, p=0.029). Peak concentration of creatine kinase myocardial fraction was lower in the GW group than in the control group (326.6+/-41.5 vs 454.9+/-46.2 mg/dl, p=0.043). GW patients showed greater improvement at 3 weeks after PCI in terms of LV ejection fraction (+4.6+/-1.2 vs -1.1+/-1.5, p=0.004), LV end-systolic volume index (+0.5+/-2.4 vs +9.0+/-2.7, p=0.023), and regional wall motion abnormalities (-2.03+/-0.14 vs -2.51+/-0.14, p=0.018). CONCLUSION: Primary stenting with GW protection can restore epicardial coronary flow and myocardial perfusion, and also preserve LV function in anterior AMI.

[Transient retinopathy after acute myocardial infarction treated by reperfusion therapy: clinical background and manifestation].

OBJECTIVES: The severe inflammatory reaction caused by acute myocardial infarction and reperfusion affects both the heart and other remote organs. The occurrence of retinopathy was evaluated in patients with acute myocardial infarction who underwent reperfusion therapy. METHODS: We investigated 29 patients with first acute myocardial infarction who underwent successful reperfusion therapy within 24 hr of the onset. Ophthalmic examinations including visual acuity test and ocular fundoscopy were performed within 3 days, 2 weeks, and then monthly up to 3 months after the onset of acute myocardial infarction. Plasma levels of intercellular adhesion molecule-1(ICAM-1), interleukin-6 and high sensitivity C-reactive protein were measured on admission. RESULTS: Soft exudates around the optic disc appeared in 17(58.6%) of the 29 patients, among whom 5 also developed superficial hemorrhages(17.2%). The retinopathy became most remarkable between 1 to 2 months after the onset of acute myocardial infarction and then faded away without any specific treatment. None of the patients had impairment of visual acuity, although 4 of the 17 patients with retinopathy complained of either blurred vision or metamorphopsia. Hypertension and/or diabetes mellitus tended to be more common in the retinopathy group than in the non-retinopathy group(59% vs 33%, p = 0.096). Plasma ICAM-1 levels were significantly higher than in the non-retinopathy group than in the retinopathy group(p = 0.017). There was no significant difference in plasma levels of interleukin-6 and high sensitivity C-reactive protein between the two groups. CONCLUSIONS: Retinopathy may occur after reperfusion for acute myocardial infarction. The dominant manifestation is transient soft exudates reflecting spotty retinal ischemia, probably due to microvascular obstruction.

Long-term prognosis of fulminant myocarditis rescued by percutaneous cardiopulmonary support device.

BACKGROUND: The long-term prognosis and cardiac function of fulminant myocarditis treated with percutaneous cardiopulmonary support (PCPS) was compared with the outcome of those not treated with PCPS. METHODS AND RESULTS: From 1991 to 2000, 14 patients with fulminant myocarditis (left ventricle ejection fraction (LVEF) < or =40%) were admitted to hospital. PCPS was necessary for treatment of shock in 8 (PCPS group), but not for the remaining 6 patients (non-PCPS group). In the PCPS group, 6 patients (75%) survived the critical phase and did not have any cardiac problems after discharge (range of follow-up period, 1.4-6.0 years). All patients in the non-PCPS group survived the acute phase; 1 patient had congestive heart failure 1.5 years after discharge, and another died from malignancy (follow-up period range, 2.2-9.4 years). Although the left ventricular ejection fraction (LVEF) of the PCPS group was significantly lower than that of the non-PCPS group in the acute phase, there was no significant difference in LVEF between the 2 groups in the chronic phase. CONCLUSION: Patients who survive the acute phase crisis of acute myocarditis have a favorable long-term survival rate, whether or not mechanical support is used.