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Background: Statin treatment has been shown to reduce the risk of coronary artery disease and improve the outcome of patients with acute myocardial infarction. However, the effects of previous statin treatment on the clinical course of subsequent acute myocardial infarction remain unclear. This study was designed to investigate whether previous statin therapy influences the clinical outcome of patients with ST-Segment Elevation Myocardial Infarction (STEMI) treated with primary Percutaneous Coronary Intervention (PCI). Methods: We evaluated the clinical outcome of 350 patients with STEMI undergoing primary PCI, of which 91 received previous statin treatment (statin group) and 259 did not (non-statin group). Myocardial perfusion, infarct size, inflammatory responses, and Major Adverse Cardiovascular Events (MACE) were evaluated. Results: The frequency of MACE at 1 month after PCI was significantly lower in the statin group than the nonstatin group (4.4% vs. 13.9%, p=0.014). Post-PCI peak creatine kinase was significantly lower in the statin group median, (interquartile range): (1246 [504-3301] vs. 2235 [952-4083] IU/ml; p=0.002), whereas peak high-sensitivity C-reactive protein did not significantly differ between the two groups (p=0.287). The frequency of ST-segment resolution after PCI was significantly higher in the statin group (90.1% vs. 76.8%; p=0.006), as was the frequency of Thrombolysis in Myocardial Infarction grade 3 coronary flow (p=0.008). Myocardial blush grade was similar in both groups (p=0.839). Multivariate logistic regression analysis revealed previous statin treatment, hs-CRP, blood glucose, and age to be independent predictors of MACE. Conclusion: Previous statin therapy enhances coronary flow, reduces infarct size, and improves clinical outcome of STEMI patients treated with primary PCI.

Pioglitazone has been shown to reduce the occurrence of fatal and nonfatal myocardial infarction (MI) in type 2 diabetes mellitus (DM). However, the mechanisms of such favorable effects remain speculative. The aim of this study was to investigate the effect of pioglitazone on arterial baroreflex sensitivity (BRS) and muscle sympathetic nerve activity (MSNA) in 30 DM patients with recent MI. Patients were randomly assigned to those taking pioglitazone (n = 15) and those not taking pioglitazone (n = 15) at 4 weeks after the onset of MI. BRS, MSNA, calculated homeostasis model assessment of insulin resistance index (HOMA-IR), and plasma adiponectin were measured at baseline and after 12 weeks. Pioglitazone increased plasma adiponectin (from 6.9 ± 3.3 μg/dL to 12.2 ± 7.1 μg/dL) and reduced HOMA-IR (from 4.0 ± 2.2 to 2.1 ± 0.9). In the pioglitazone group, MSNA decreased significantly (from 37 ± 7 bursts/min to 25 ± 8 bursts/min) and BRS increased significantly (from 6.7 ± 3.0 to 9.9 ± 3.2 ms/mm Hg) after 12 weeks. Furthermore, a significant relationship was found between the change in MSNA and HOMA-IR (r = 0.6, P = 0.042). Thus, pioglitazone decreased the sympathetic nerve traffic through the improvement of insulin resistance in DM patients with recent MI, which indicate that the sympathoinhibitory effects of pioglitazone may, at least in part, have contributed to the beneficial effects of pioglitazone.

Background Pre-hospitalization medication such as aspirin and nitrates has been shown to affect the mode of presentation in acute coronary syndrome (ACS). However, it is not formally assessed whether other cardiovascular medications may be contributed to the differences in the mode of presentation, especially in relation to coronary risk factors. Methods and results We conducted a registration study of patients (M/F 850/323) with either ST-segment elevation myocardial infarction (STEMI), non-ST-segment elevation myocardial infarction (NSTEMI) or unstable angina (UA), and examined the differences in the mode of presentation, pre-hospitalization medication, and coronary risk factors. The ratio of the incidence of STEMI and NSTEMI/UA was significantly reduced in patients having pre-hospitalization medication with aspirin, nitrates or statins, but not with other medications such as beta-blockers in multivariate analysis. Pre-hospitalization medication with aspirin and nitrates was significantly associated with the same reduction of the ratio in patients with male gender, hypertension, diabetes mellitus and a history of coronary artery disease. However, in patients who smoked, were obese and hypercholesterolemic, pre-hospitalization medication with nitrates was significantly associated with the reduced ratio. The ratio was significantly low in patients with males and hypercholesterolemia treated with statins before admission. Conclusion Depending on their coronary risk factors, pre-hospitalization medication with aspirin, nitrates or statins was associated with a different presentation and evolution of ACS.

A 42-year-old man was referred to our hospital for an electrophysiologic study because of recurrent episodes of palpitation. On coronary angiogram, an anomalous atresia of the coronary sinus (CS) ostium was discovered. The ablation catheter was inserted from the right femoral artery to the accessory pathway (AP) of posterior paraseptal area. The earliest retrograde atrial activation was recorded in the 5-6 o'clock region of the mitral annulus. Radiofrequency energy was delivered to this site, resulting in elimination of the AP. After this application, there was persistent ventriculoatrial dissociation and led to successful ablation of the AP.

Contrast-induced nephropathy (CIN) is associated with increased morbidity and mortality rates. Although a previous study reported that pretreatment with sodium bicarbonate is more effective than sodium chloride for prophylaxis of CIN, this has not been a universal finding. We performed a prospective randomized trial to investigate whether CIN can be avoided using sodium bicarbonate. In total 155 patients with a glomerular filtration rate (GFR)

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.

Sympathetic nerve overactivity and reduced exercise tolerance are characteristic features of patients with heart failure. However, to what extent sympathetic nerve overactivity contributes to limiting exercise tolerance has not been clearly defined. Myocardial iodine 123-metaiodobenzylguanidine (MIBG) scintigraphy, muscle sympathetic nerve activity (MSNA), and cardiopulmonary exercise testing were performed within 3 days in 30 patients with left ventricular dysfunction (LVD). Cardiac sympathetic nerve activity was estimated using H/M ratio and washout rate (WR) of 123I-MIBG imaging. MSNA was recorded by microneurography. The patients with peak VO2

Objective: This study examined the cardiovascular adaptations of an exercise training program and evaluated the role of peripheral vasodilator capacity in contributing to these adaptations after myocardial infarction. Design: A total of 44 consecutive patients with uncomplicated myocardial infarction underwent 3 wks of exercise training. Controls (n = 12) with comparable myocardial infarction were selected from our database and were restricted to a program with minimal activity. All patients performed cardiopulmonary exercise testing with hemodynamic measurements. Forearm and calf reactive hyperemic flow were measured by venous occlusive plethysmography as indices of peripheral vasodilator capacity. Results: Despite no change in arteriovenous oxygen difference at peak exercise after training, training resulted in significant increases in oxygen consumption, cardiac output, and stroke volume and a significant decrease in systemic vascular resistance at peak exercise (overall, P < 0.05). Calf reactive hyperemic flow increased significantly after training (P < 0.001), but forearm reactive hyperemic flow did not. Furthermore, increase in calf reactive hyperemic flow after training had a positive correlation with increases in peak cardiac output, stroke volume, and oxygen consumption after training and an inverse correlation with peak systemic vascular resistance. Conclusions: Exercise training improved exercise tolerance by improving hemodynamic responses to exercise after myocardial infarction. This improved exercise performance was linked to a training-induced increase in calf vasodilator capacity.

To examine the relationship among heart rate turbulence parameters, arterial baroreflex sensitivity, and cardiac sympathetic nerve activity, 15 patients with acute myocardial infarction, presenting with sinus rhythm andor = 3 ventricular premature beats/24 hr were studied at least 2 weeks after acute myocardial infarction. Turbulence onset (TO) and turbulence slope (TS) were averaged from 3 respective ventricular premature beats. Early heart-to-mediastinum ratio (H/M), delayed H/M, and washout rate were calculated from iodine-123-metaiodobenzylguanidine (123I MIBG) scintigraphy. Arterial baroreflex sensitivity was calculated by phenyrephrine method. Arterial baroreflex sensitivity correlated significantly with TO (r = - 0.75, p.01) and TS (r = 0.53, p.05). TO had no correlations with early H/M, delayed H/M, and washout rate. There were no significant correlations between TS and early H/M. However, TS had significant correlation with delayed H/M (r = 0.74, p.01) and washout rate (r = -0.71, p.01). Thus, heart rate turbulence of TO and TS parameters depend on sympathovagal balance.

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.

Study objective: To assess the effect of coronary flow to the infarct zone before primary coronary angioplasty on hospital complications in patients with acute myocardial infarction (MI). Design: Consecutive case series analysis. Setting: Coronary-care unit in a university hospital. Patients: Two hundred sixty-four consecutive patients with ST-elevation acute MIs who had successful primary percutaneous transluminal coronary angioplasty. Interventions: Coronary angiography on hospital admission and serial echocardiography. Measurements and results: The status of infarct-related artery flow before primary angioplasty was evaluated on hospital admission. Left ventricular wall motion and pericardial effusions were studied by echocardiography. One hundred ninety patients had total occlusions (Thrombolysis in Myocardial Infarction [TIMI] flow grade, 0 to 1) in the infarct-related artery (group 1), and 74 patients had antegrade flow (TIMI flow grade, 2 to 3) [group 2] before undergoing primary angioplasty procedures. When group 1 was subdivided into two groups (for the presence and absence of collateral flow), the patients with total occlusions and no collateral flow had a higher incidence of left ventricular aneurysmal wall motion (11% vs 1%, respectively; p 0.03) and pericardial friction rub (15% vs 3%, respectively; p 0.03) than did those in group 2. Moreover, those patients with total occlusions and no collateral flow had higher incidences of pericardial effusion (34% vs 17%, respectively; p 0.02; and 34% vs 9%, respectively; p < 0.01) and in-hospital mortality (8% vs 1%, respectively; p 0.04; and 8% vs 1%, respectively; p 0.06) than did those patients in the other two groups. Conclusions: Despite successful primary angioplasty, the absence of antegrade flow in the infarct-related artery and collateral flow to the infarct zone before angioplasty resulted in a higher incidence of in-hospital complications. (CHEST 2001; 120:1959 –1963)

We evaluated the effect of angiotensin-converting enzyme inhibition (quinapril) on cardiopulmonary baroreflex sensitivity in 30 patients with uncomplicated myocardial infarction (quinapril group, 15 patients; placebo group, 15 patients) at 5 and 10 days after the onset of myocardial infarction. This study indicates that quinapril improved cardiopulmonary baroreflex and thus reduced sympathetic outflow in patients with acute myocardial infarction.

Distribution of skeletal muscle perfusion during exercise is an important factor in determining exercise capacity and is markedly impaired in patients with cardiac disease. This study examined the importance of intrinsic calf vasodilator capacity in determining distribution of skeletal muscle perfusion during supine bicycle exercise in patients with left ventricular dysfunction.We studied 19 patients with left ventricular dysfunction (left ventricular ejection fraction45%) after myocardial infarction. All the patients underwent cardiopulmonary exercise testing with measurements of central hemodynamics, leg blood flow (LBF), and the percentage of cardiac output distributed to both legs (%LBF). Calf reactive hyperemic flow (RH) was measured by venous occlusive plethysmography at supine rest.LBF at peak exercise was closely related to peak cardiac output and RH. Furthermore, %LBF at peak exercise had modest correlation with peak cardiac output and good correlation with RH. Although peak cardiac output and RH were independent determinants of LBF at peak exercise by multiple regression analysis, RH had higher correlation with %LBF at peak exercise than peak cardiac output. Despite marked changes in other hemodynamic variables, nonleg blood flow during exercise was constantly maintained at a level identical to resting value.Calf vasodilator capacity, which was the major determinant of distribution of skeletal muscle perfusion during exercise, may have contributed to maintaining perfusion of important nonexercising regions during exercise in patients with left ventricular dysfunction.

To examine the relation between left atrial (LA) function and exercise performance.Retrospective study at a referral cardiopulmonary exercise laboratory in a university hospital.Forty-one patients with recent myocardial infarction.M-mode echocardiography and cardiopulmonary exercise testing combined with radionuclide ventriculography.Hemodynamic measurements were obtained at rest and peak exercise. LA fractional shortening at rest was used as an index of global LA function. LA fractional shortening had fair correlations with peak oxygen consumption (r=0.67, p0.01) and exercise duration (r=0.71, p0.01). Although there were no significant relations between LA fractional shortening and hemodynamic measurements at rest, LA fractional shortening was positively related to peak cardiac output (r=0.61, p0.01) and peak stroke volume (r=0.57, p0.01), and negatively related to peak pulmonary arterial wedge pressure (r=-0.44, p0.05). In addition, LA fractional shortening correlated significantly with an increase in left ventricular (LV) end-diastolic volume from rest to peak exercise (r=0.48, p0.02), but did not correlate with the changes in ejection fraction and end-systolic volume during exercise. An increase in LV end-diastolic volume during exercise was significantly related to peak oxygen consumption (r=0.46, p0.02), peak cardiac output (r=0.60, p0.01), and peak stroke volume (r=0.53, p0.01), whereas the changes in ejection fraction and end-systolic volume during exercise were not related to these indexes.Exercise capacity and LV performance during exercise were mainly dependent on LV diastolic filling rather than systolic contraction during exercise. LA fractional shortening at rest reflected LV diastolic filling during exercise and, therefore, predicted cardiac output and stroke volume responses to exercise and exercise capacity in patients with recent myocardial infarction.

To investigate the role of left ventricular (LV) diastolic function in the maintenance of exercise capacity in patients with systolic dysfunction, symptom-limited cardiopulmonary exercise testing combined with radionuclide ventriculography was performed in 24 patients with an LV ejection fraction < 35% after anterior myocardial infarction. The ratio of pulmonary artery wedge pressure (PAWP) to LV end-diastolic volume (EDV), an index of global diastolic function, correlated significantly with peak oxygen consumption at peak exercise (r = -0.55; p = 0.006), whereas ejection fraction at peak exercise did not. The change in PAWP/EDV ratio from rest to peak exercise was related to the increases in stroke volume (r = -0.54; p = 0.006) and cardiac output (r = -0.51; p = 0.01) during exercise, but the change in ejection fraction was not. Resting hemodynamics did not differ between patients with preserved exercise capacity (group 1, n = 8) and those with exercise impairment (group 2, n = 16). At peak exercise, stroke volume, cardiac output, and EDV were significantly higher, and PAWP and PAWP/EDV ratio were significantly lower in group 1 than in group 2, but ejection fraction and end-systolic volume were similar in both groups. Although the incidences of hypertension, LV hypertrophy, and infarct-related coronary artery lesions did not differ between the two groups, group 2 had a significantly higher incidence of non-infarct-related coronary artery lesions than group 1 (p < 0.05). Thus in patients with LV systolic dysfunction after anterior myocardial infarction, the major cause of exercise impairment and failure to increase LV performance during exercise was diastolic dysfunction associated with the presence of non-infarct-related coronary artery lesions with the potential for exercise-induced ischemia of the noninfarcted areas.

To examine the effects of left ventricular (LV) diastolic dysfunction on exercise capacity, hemodynamic and radionuclide responses were measured at rest and during exercise in 50 patients with recent myocardial infarction. The ratio of an increase in pulmonary arterial wedge pressure (PAWP) to an increase in LV end-diastolic volume (EDV) from rest to peak exercise (delta PAWP/delta EDV) was used as an index of LV diastolic function, delta PAWP/delta EDV had modest and negative correlations with peak oxygen consumption (VO2), cardiac output, and stroke volume in all patients. Among patients with peak VO2or = 20 ml/min/kg (group I, n = 24) and those with peak VO220 ml/min/kg (group II, n = 26), there were no differences between the 2 groups with regard to resting LV ejection fraction, EDV, PAWP, cardiac output, and stroke volume. Although there was no significant difference in LV ejection fraction at peak exercise, group II had significantly reduced EDV, increased PAWP, and decreased cardiac output and stroke volume than those in group I. As a result, delta PAWP/delta EDV was significantly higher in group II. These results suggest that LV diastolic dysfunction has a key role in determining exercise capacity in patients with reduced exercise capacity after recent myocardial infarction.

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.

To evaluate the difference in left ventricular (LV) pump function during predischarge exercise testing between postmenopausal women and age-matched men with myocardial infarction, global and regional ejection fraction, LV end-diastolic volume, and the ratio of systolic blood pressure to LV end-systolic volume were investigated using radionuclide angiography in 25 postmenopausal women and 37 age-matched men. There were no significant differences in the resting radionuclide angiographic indexes between women and men. Global and regional ejection fraction of noninfarcted area, and the ratio of systolic blood pressure to LV end-systolic volume decreased at peak exercise in women, but these indexes increased in men. Although there was no significant difference in the amount of change in LV end-diastolic volume during exercise between the 2 groups, the amount of increase in LV end-systolic volume was significantly larger in women than in men. The ratio of systolic blood pressure to LV end-systolic volume had a curvilinear relation with LV end-diastolic volume at rest and peak exercise, but the ratio of systolic blood pressure to LV end-systolic volume was larger at any LV end-diastolic volume in men than in women during exercise. Thus, lower global ejection fraction and the ratio of systolic blood pressure to LV end-systolic volume during exercise in postmenopausal women compared with age-matched men indicate that gender may have played an important role in the LV remodeling process.

It is often difficult to noninvasively differentiate a post-infarction left ventricular (LV) pseudoaneurysm from a post-infarction true aneurysm. A 66-year-old woman with a past history of inferior acute myocardial infarction was admitted to our hospital because of acute decompensated heart failure. Two-dimensional transthoracic echocardiography showed an aneurysm with a narrow orifice in the inferoposterior basal area. The pulmonary to systemic flow ratio (Q p/Q s) was 2.2:1, which corresponded to moderate left–right shunting. Three-dimensional transesophageal echocardiography (3D-TEE) showed the orifice in the perforated right ventricular basal area with a color jet through the orifice from the LV to the right ventricle. Collectively, based on the 3D-TEE findings, we diagnosed the case as inferoposterior pseudoaneurysm with a left-to-right shunt caused by myocardial infarction.

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.

To assess the difference in left ventricular performance during exercise between anterior (11 patients) and inferior (10 patients) myocardial infarction (MI) of equivalent size, patients performed a supine bicycle exercise 6 to 8 weeks after the first acute MI. All patients had negative exercise test results and despite no significant differences in HR, blood pressure and stroke volume index at peak exercise, pulmonary artery wedge pressure was significantly higher in anterior (35 +/- 7 mm Hg) than in inferior MI (27 +/- 9 mm Hg). Although there were no significant differences in electromechanical systole (QS2) and diastolic time (DT) at rest, a significant prolongation of QS2 with consequent shortening of DT (p0.01) was observed at peak exercise in anterior MI. In addition to decreased subendocardial coronary blood flow from increased left ventricular end-diastolic pressure, a disproportionate shortening of DT in anterior MI may initiate subendocardial ischemia in the noninfarcted segments, which may further impede subendocardial blood flow.

Changes in left ventricular (LV) ejection rate were evaluated during supine bicycle exercise and recovery in 12 patients with anterior myocardial infarction. Pulmonary artery wedge pressure (34 +/- 9 to 14 +/- 5 mm Hg) and plasma norepinephrine level decreased at 2 min recovery from peak exercise, whereas plasma lactate tended to increase. As a result, LV ejection rate reached the highest value at 2 min of recovery. Thus, both cardiac (optimal filling pressure) and peripheral factors (reduced vascular resistance) caused the increase in LV ejection rate at early recovery.

Summary Background: Clonidine is a potent sympatholytic drug with central neural effects. The aim of this study was to evaluate the effects of clonidine on arterial baroreflex sensitivity (BRS) and cardiopulmonary (CP) baroreflex control of muscle sympathetic nerve activity (MSNA) in patients with left ventricular (LV) dysfunction. Method: Twenty patients were randomly assigned to either clonidine or placebo groups (10 in each group). BRS (by phenylephrine method) and CP baroreflex (by lower body negative pressure) effects on sympathetic nerve activity (circulating norepinephrine and MSNA recordings) were measured before and after a 4-week treatment period. Results: Clonidine lowered blood pressure and heart rate. Clonidine was accompanied not only by a decrease in plasma noradrenaline (from 444 ± 196 to 260 ± 144 pg ml−1) but also by a reduction in directly measured MSNA (from 47 ± 16 to 36 ± 16 bursts min−1). BRS increased significantly from 3·01 ± 1·19 to 6·86 ± 2·84 ms mmHg−1 after clonidine. When expressed as per cent change in MSNA during CP baroreceptor stimulation, CP baroreflex control of MSNA was significantly increased from 9·26 ± 8·93% to 28·83 ± 11·96% after clonidine. However, there were no significant changes in the measured variables in the control group. Conclusion: Clonidine enhanced BRS and CP baroreflex control of MSNA while reducing baseline sympathetic activity in patients with LV dysfunction.

SUMMARY To investigate the relationship between arterial baroreflex sensitivity (BRS) and exercise capacity, we examined arterial BRS and its relation to exercise capacity during upright bicycle exercise in 40 uncomplicated patients with acute myocardial infarction. Arterial BRS was measured 3 weeks (20 +/- 5 days) after acute myocardial infarction and assessed by calculating the regression line relating phenylephrine-induced increases in systolic blood pressure to the attendant changes in the R-R interval. All patients underwent graded symptom-limited bicycle exercise with direct measurements of hemodynamic and metabolic measurements. In all patients, the average arterial BRS was 5.6 +/- 2.6 ms mmHg(-1). There were no significant correlations between arterial BRS and hemodynamic measurements at rest. However, arterial BRS was negatively related to systemic vascular resistance at peak exercise (r = -0.60, P = 0.0001) and percent change increase in systemic vascular resistance from rest to peak exercise (r = -0.45, P = 0.003), whereas arterial BRS was positively related to cardiac output (r = -0.48, P = 0.002) and stroke volume at peak exercise (r = 0.42, P = 0.007), and percent change increase in cardiac output (r = -0.55, P = 0.0002) and stroke volume from rest to peak exercise (r = 0.41, P = 0.008). Furthermore, arterial BRS had modest but significant correlations with peak oxygen consumption (r = -0.48, P = 0.002) and exercise duration (r = 0.35, P = 0.029), indicating that patients with better arterial BRS have better exercise capacity in patients with acute myocardial infarction. These results suggest that arterial BRS was linked to central and peripheral hemodynamic responses to exercise and hence, contributed to exercise capacity after acute myocardial infraction.

To elucidate the role of inflammatory and hemodynamic factors in the genesis of atrial fibrillation in acute myocardial infarction, 228 patients with a first Q wave anterior myocardial infarction were studied. Forty-nine patients had pericarditis (detection of pericardial rub by careful auscultation), and 36 patients had echocardiographically demonstrated hydropericardium (presence of pericardial effusion without pericardial rub). During the first 3 days after admission, transient episodes of atrial fibrillation were observed in 10 patients (20%) with pericarditis (group 1), 15 patients (42%) with hydropericardium (group 2), and 20 patients (14%) without pericarditis and hydropericardium (group 3). Although there was no significant difference in the incidence of atrial fibrillation between groups 1 and 3, patients in group 2 had a significantly higher incidence of atrial fibrillation than those in groups 1 and 3. Pulmonary capillary wedge pressure and the number of advanced asynergic segments were found to be the important factors discriminating the three groups by multivariate analysis. Therefore atrial fibrillation after acute Q wave anterior infarction was not related to the inflammatory infiltration involving the atria but to the increase in atrial pressure resulting from hemodynamic change caused by more extensive myocardial damage.

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.

Exercise training has been shown to favorably affect the prognosis after acute myocardial infarction (AMI), but the mechanisms of such favorable effects remain speculative. The aim of this study was to determine whether exercise training improves baroreflex control of heart rate and muscle sympathetic nerve activity (MSNA) in patients with AMI.Prospective randomized clinical study.Thirty patients with an uncomplicated AMI were randomized into trained or untrained groups. Arterial BP, heart rate, and MSNA were measured at rest, and during baroreceptor stimulation (phenylephrine infusion) and baroreceptor deactivation (nitroprusside infusion). These measurements were performed at baseline and after 4 weeks of exercise training.Peak oxygen uptake increased significantly (12.3 +/- 10.7% [mean +/- SD]) with exercise training. Resting MSNA reduced from 34 +/- 12 to 27 +/- 8 bursts/min in the trained group but not in the untrained group. Arterial baroreflex sensitivity (BRS) [from 8.9 +/- 3.0 to 10.3 +/- 3.0 ms/mm Hg, p0.05] and MSNA response to baroreceptor stimulation (change of integrated MSNA from - 47 +/- 23 to - 70 +/- 21%, p0.01) improved significantly in the trained group, but not in the untrained group. Despite baroreceptor deactivation improving MSNA response in both groups, there was no significant difference between the two groups.Exercise training increased arterial BRS and decreased sympathetic nerve traffic after AMI, which indicate that the sympathoinhibitory effect of exercise training may, at least in part, contribute to the beneficial effect of exercise training in patients with AMI.

Summary Background: Iodine 123-metaiodobenzylguanidine (MIBG) imaging has been used to assess cardiac sympathetic nerve abnormalities. To determine the role of MIBG imaging as a measure of generalized sympathetic nerve activity, MIBG imaging was evaluated with muscle sympathetic nerve activity (MSNA) and plasma norepinephrine (noradrenaline) level in patients with old myocardial infarction. Methods: Myocardial MIBG scintigraphy, MSNA and plasma norepinephrine measurement were performed within 3 days in 35 patients with old myocardial infarction. Patients were divided into three groups according to their ejection fraction (EF); preserved (EF ≥ 50%, 12 patients), intermediate (35%

A 71-year-old woman being treated with predonine at a dose of 10 mg/d for rheumatoid arthritis had a short episode of syncope lasting a couple of minutes. Her physical examination on admission revealed clear consciousness, resting tachycardia of 96 beats per minute, blood pressure of 114/68 mm Hg, jugular venous distention, and edema of the dorsum of the right foot. Electrocardiography revealed sinus tachycardia and right axis deviation. Chest radiography showed no pulmonary congestion. Transthoracic echocardiography showed a moderately dilated right ventricle with impaired right ventricular systolic function containing a large freefloating echogenic mass. There was moderate tricuspid regurgitation with an estimated pulmonary artery pressure of 59/24 mm Hg. Subsequent investigation by real-time 3-dimensional transesophageal echocardiography revealed that the large floating right intraventricular mass was highly mobile (Figure 1A and Video 1) and attached to the chordal structures of the tricuspid valve, which was prolapsing through the pulmonary valve into the main pulmonary artery. The clinical suspicion of pulmonary thromboembolism was subsequently confirmed by lung perfusion scanning. Anticoagulation therapy with intravenous heparin was initiated, and urgent cardiac surgery was performed with complete removal of the thrombus (Figure 1B). Histopathologic examination of the removed material showed findings consistent with a thrombus. Long-term oral anticoagula

Background This study was designed to determine the clinical significance of ST-segment elevation in the precordial leads (leads V1 and V2) in acute Q-wave inferior wall myocardial infarction. Methods and results One hundred fifty-eight consecutive patients with acute Q-wave inferior wall myocardial infarction were classified into 3 groups on the basis of the initial ST-change in V1 (group 1 = 29 patients with ST elevation, group 2 = 97 patients with ST depression, and group 3 = 32 patients with no ST-segment change). The right coronary artery was the infarct-related artery in all the patients in group 1. Although there was no significant difference between groups 1 and 2, the number of left ventricular asynergic segments was larger and the incidence of major in-hospital arrhythmias was higher in groups 1 and 2 compared with group 3. Patients in group 1 had a significantly higher incidence of proximal lesion (86%) and right ventricular infarction (69%) than the other 2 groups did. When ST elevation in leads V1 and V2 was considered, 14 of 15 patients (93%) with ST elevation only in V1 had right ventricular infarction, whereas 6 of 14 patients (43%) with ST elevation in both V1 and V2 had right ventricular infarction (P =.011). Conclusions ST-segment elevation in V1 on admission in patients with acute Q-wave inferior wall myocardial infarction indicates a right coronary artery lesion associated with a larger infarct size and a higher incidence of major in-hospital arrhythmias.

To elucidate the clinical characteristics associated with regional ventricular dilatation in the early phase of myocardial infarction (MI), 228 patients with acute Q-wave anterior MI were studied. Forty-nine patients (21 percent) had echocardiographically demonstrated regional ventricular dilatation (an abnormal bulge in the left ventricular contour during both systole and diastole) on the third hospital day. Careful auscultation revealed that a pericardial rub was present in 49 patients (21 patients with and 28 patients without regional ventricular dilatation) during the first three days after hospital admission. Multivariate analysis was performed to determine the relative importance of pericardial rub with six other clinical variables related to regional ventricular dilatation. Pericardial rub and cardiac output were the significant factors related to the presence of regional ventricular dilatation. Thus, a pericardial rub, in concert with impaired left ventricular function, is a physical sign associated with regional ventricular dilatation, and anatomically transmural infarction is the possible factor explaining their association.

Leg blood flow (LBF) and its relation to central hemodynamics were examined during recovery following maximal supine bicycle exercise in 11 patients with heart failure and 20 patients with normal exercise capacity after myocardial infarction. The results indicate that LBF was markedly reduced in patients with heart failure, and that decreased cardiac output response and enhanced peripheral vasoconstriction, which functioned to prevent hypoperfusion in the nonexercising vital regions and to maintain arterial blood pressure, were responsible for the reduced LBF during recovery in heart failure.

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.

To evaluate the change of ventriculoarterial coupling during low-level exercise in patients after myocardial infarction, the ratio of systolic blood pressure to left ventricular end-systolic volume (P/V ratio) and the ratio of systolic blood pressure to stroke volume (effective arterial elastance) were investigated using radionuclide angiography in 73 consecutive patients with a negative predischarge exercise test. The patients were divided into three groups according to their resting left ventricular ejection fraction: group A (n = 12)or = 60%; group B (n = 32) 41-59%; group C (n = 29)or = 40%. The ejection fraction increased significantly during exercise in all three groups. There was no significant difference in the change of the P/V ratio during exercise between groups A and B, but it was significantly smaller in group C. The effective arterial elastance increased during exercise in group A, did not change in group B, and decreased in group C. Thus, the augmentation of myocardial contractility was an important factor related to the increase in ejection fraction during exercise in patients with normal or slightly reduced cardiac function, whereas the decrease in effective arterial elastance was important in patients with poor cardiac function.

The pattern of oxygen (O2) consumption (VO2), carbon dioxide (CO2) production (VC02), ventilatory and metabolic responses during and in recovery from supine bicycle exercise was examined in 18 patients with recent myocardial infarction. An increase in VO2 with increasing work load was accomplished by proportional increases in both cardiac output and the arteriovenous O2 difference. During recovery, however, the arteriovenous O2 difference rapidly decreased below levels at rest, whereas VO2 and cardiac output remained elevated, indicating that VO2 during recovery further depended on relatively high cardiac output. The ratio of VCO2 to VO2 further increased after exercise, suggesting that such cardiac output contributed to the remaining high CO2 flow to the lung and therefore enhanced ventilation. Increased arterial catecholamines during exercise remained elevated for the first 5 minutes of recovery. Arterial lactate during this period continued to increase and resulted in profound metabolic acidosis, causing alveolar hyperventilation after exercise. These results suggest that during recovery from exercise, cardiopulmonary responses remain enhanced because of continuing high cardiac output, resulting in subsequent high CO2 flow to the lung and metabolic acidosis, and that this may be associated with profound fatigue or dyspnea after exercise.

Purpose: The aim of this study was to examine the influence of diastolic function on angiotensin II type I receptor blocker (ARB) in patients with mild left ventricular (LV) dysfunction already treated with angiotensin converting enzyme (ACE) inhibitors. Method: Diastolic function and neurohumoral variables were evaluated in 15 patients with mild LV dysfunction already treated with ACE inhibitors before and 4 weeks after administration of the ARB, telmisartan 40 mg. Diastolic function was determined by Doppler derivatives of mitral inflow (E/A ratio, deceleration time of early inflow) and pulmonary venous flow velocity (S/D ratio). B-natriuretic peptide (BNP), alpha-human atrial natriuretic peptide (HANP), plasma renin and plasma aldosteron were measured. Result: Arterial blood pressure decreased significantly after telmisartan (p 0.01). MV-E/A, deceleration time and isovolmic relaxation time did not changed after telmisartan. But pulmonary venous flow velocity improved significantly from 43 4 from 37 3 after telmisartan (p 0.05). Moreover, BNP decreased significantly from 143 85 to 76 47 pg/mL after telmisartan (p 0.05). Plasma renin, plasma aldosteron and HANP did not change after telmisartan. Conclusion: ARB telmisartan improves diastolic dysfunction in patients with mild LV dysfunction already treated with ACE inhibitors.

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