Wearing Compression Garment after Endurance Exercise Promotes Recovery of Exercise Performance.

The present study examined the effects of wearing a lower-body compression garment (CG) after endurance exercise on recovery of physiological function. 18 males were divided into 2 experiments, the downhill running (n=10, DHR) experiments and the level running (n=8, LR) experiments. Subjects performed 30 min of DHR (gradient: - 10%) or LR (gradient: 0%) at 70% of ˙VO2max with either wearing a CG (CG trial) or normal garment (CON trial) for 24 h after running. Changes in jump performance (counter movement jump; CMJ, rebound jump; RJ, drop jump; DJ), subjective feelings, circumferences of leg, and blood variables (creatine kinase, myoglobin, interleukin-6, high-sensitivity C-reactive protein) were evaluated before exercise, immediately after exercise, 1, 3 and 24 h following exercise. Running economy was evaluated at 24 h following exercise. CMJ height and RJ index were significantly higher in the CG trial than in the CON trial 24 h after running (P<0.05). Although changes in muscle soreness and blood variables were significantly greater in the DHR experiment than in the LR experiment, there was no significant difference between the trials in either experiment. Wearing a CG following endurance exercise facilitated recovery of jump performance under situations with severe exercise-induced muscle damage.

Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. Angina Pectoris-Myocardial Infarction Investigations in Japan.

OBJECTIVES: To determine the clinical features of a novel heart syndrome with transient left ventricular (LV) apical ballooning, but without coronary artery stenosis, that mimics acute myocardial infarction, we performed a multicenter retrospective enrollment study. BACKGROUND: Only several case presentations have been reported with regard to this syndrome. METHODS: We analyzed 88 patients (12 men and 76 women), aged 67 +/- 13 years, who fulfilled the following criteria: 1) transient LV apical ballooning, 2) no significant angiographic stenosis, and 3) no known cardiomyopathies. RESULTS: Thirt-eight (43%) patients had preceding aggravation of underlying disorders (cerebrovascular accident [n = 3], epilepsy [n = 3], exacerbated bronchial asthma [n = 3], acute abdomen [n = 7]) and noncardiac surgery or medical procedure (n = 11) at the onset. Twenty-four (27%) patients had emotional and physical problems (sudden accident [n = 2], death/funeral of a family member [n = 7], inexperience with exercise [n = 6], quarreling or excessive alcohol consumption [n = 5] and vigorous excitation [n = 4]). Chest symptoms (67%), electrocardiographic changes (ST elevation [90%], Q-wave formation [27%] and T-wave inversion [97%]) and elevated creatine kinase (56%) were found. After treatment of pulmonary edema (22%), cardiogenic shock (15%) and ventricular tachycardia/fibrillation (9%), 85 patients had class I New York Heart Association function on discharge. The LV ejection fraction improved from 41 +/- 11% to 64 +/- 10%. Transient intraventricular pressure gradient and provocative vasospasm were documented in 13/72 (18%) and 10/48 (21%) of the patients, respectively. During follow-up for 13 +/- 14 months, two patients showed recurrence, and one died suddenly. CONCLUSIONS: A novel cardiomyopathy with transient apical ballooning was reported. Emotional or physical stress might play a key role in this cardiomyopathy, but the precise etiologic basis still remains unclear.

Myocardial contractile efficiency and oxygen cost of contractility are preserved during transition from compensated hypertrophy to failure in rats with salt-sensitive hypertension.

In Dahl-Iwai rats, salt-sensitive hypertension causes concentric left ventricular hypertrophy (LVH) at the age of 11 weeks, which is followed by LV dilatation with global hypokinesis and pulmonary congestion, ie, LV failure (LVF), at 16 to 18 weeks of age. To address the question of whether the cardiac remodeling from LVH to LVF is associated with modulations of mechanoenergetic properties, we serially measured the LV pressure-volume area (PVA) and myocardial oxygen consumption (MVO2) in isolated, isovolumically contracting hearts from this animal model. The end-systolic pressure-volume relationships obtained by stepwise changes of the LV volume were fit into a binominal regression model, which provided a value of LV contractility (E(es)) and a volume intercept (V0). A slope (the reciprocal of the LV contractile efficiency) and a PVA-independent MVO2 were determined by a regression analysis of the MVO2-PVA relation. The procedure was repeated at different Ca2+ concentrations in perfusate to estimate the oxygen cost of contractility (dMVO2/dE(es)). The MVO2 was further evaluated during K+-induced cardiac arrest to delineate the basal metabolism, which was independent of the E-C coupling. During the transition from LVH to LVF, the E(es) was decreased by 50% (from 681 to 338 mm Hg x g x mL(-1), P<.001), which was associated with a substantial increase in V0 (from 0.002 to 0.07 mL, P<.01). These alterations in both the inotropic state and the ventricular shape were associated with a 45% decrease in the PVA-independent MVO2 (from 800 to 440 mL O2 x beat(-1) x g(-1), P<.01). Despite these marked changes between the two stages, both the LV contractile efficiency and the oxygen cost of contractility remained unchanged. The MVO2 during cardiac arrest also showed an equal level among the groups; hence, from LVH to LVF, the nonmechanical O2 consumption by the E-C coupling decreased in a manner parallel to the basal contractile state. We conclude that (1) in this animal model, the heart failure transition is associated with a marked decrease in myocardial contractility and with ventricular remodeling; (2) despite these changes, the efficiency of the chemomechanical conversion is highly preserved; and consequently, (3) the total energy consumption per unit of failing myocardium is diminished along with its reduced nonmechanical energy expenditure for E-C coupling. These mechanoenergetic properties might constitute an adaptive mechanism in the energy-starved condition of chronically diseased myocardium.

Previous angina reduces in-hospital death in patients with acute myocardial infarction.

There is little information on how previous angina influences in-hospital deaths secondary to acute myocardial infarction (MI). This study evaluated the causes of in-hospital deaths in MI patients with and without previous angina. A total of 2,264 consecutive patients were admitted to our hospital due to acute MI. These patients were divided into 2 groups according to the presence or absence of prior MI. Both groups were further divided according to the presence or absence of previous angina. The causes of in-hospital deaths were classified into 4 categories: (1) cardiogenic shock or congestive heart failure, (2) cardiac rupture, (3) arrhythmia, and (4) other causes. In patients with a first MI, the in-hospital mortality rate was lower in patients with previous angina than those without (6.9% vs 11.4%, p <0.01). There was no significant difference between these patients with and without previous angina in in-hospital deaths due to cardiogenic shock or congestive heart failure, arrhythmia, or other causes. Death due to cardiac rupture was less frequent in patients with previous angina (1.4% vs 5.0%, p <0.01). In patients with prior MI, the in-hospital mortality rate was lower in patients with than without previous angina (17.7% vs 25.3%, p <0.05). In contrast to patients with their first MI, there was a trend toward a lower incidence of in-hospital death due to cardiogenic shock or congestive heart failure in patients with previous angina (12.8% vs 19.0%, p = 0.05). There were no significant differences in in-hospital deaths due to cardiac rupture, arrhythmia, and other causes between the 2 subgroups. In multivariate analysis, previous angina was an independent predictor of in-hospital death. Thus, in-hospital deaths after acute MI in patients with previous angina were less because of less cardiac rupture in patients with a first MI and less cardiogenic shock or congestive heart failure in patients with prior MI.

Effect on survival of previous angina pectoris after acute myocardial infarction.

Although the present study revealed that previous angina improved in-hospital outcome, no further benefit was observed once the patients left the hospital. The worse long-term prognosis was associated with multi-vessel coronary disease in patients with previous angina.

Usefulness of serum troponin T levels on day three or four in predicting survival after acute myocardial infarction.

The appearance of serum troponin T (tn-T) on day 1 after acute myocardial infarction (AMI) strongly depends on coronary reperfusion. In contrast, the kinetics of tn-T release after day 1 after AMI are unaffected by the reperfusion status, and reflect the degradation of myofilaments in irreversibly damaged cells. However, it is not known whether serum tn-T levels after day 1 after AMI can be used to predict the long-term outcome. The purpose of this study was to elucidate the prognostic value of determining the tn-T level on day 3 or 4 after AMI. Serum tn-T levels on day 3 or 4 after AMI were measured in 121 patients (92 men and 29 women, mean age 65 years). Mean follow-up period was 526 days. There were 12 deaths (9 cardiac and 3 noncardiac) during the follow-up period. By Kaplan-Meier analysis, patients with tn-T levels higher than the median level (6.9 ng/ml) had a significantly higher mortality rate than those with submedian levels (p <0.01). By multivariate Cox proportional-hazards regression analysis, the serum tn-T level was an independent predictor of the long-term outcome after AMI (p <0.01). Futhermore, in patients with a first AMI, the serum tn-T level exhibited a significant negative linear correlation with left ventricular ejection fraction assessed 4 weeks after AMI (r = -0.48, p <0.001). Increased serum tn-T levels on day 3 or 4 after AMI are a powerful noninvasive predictor of poor long-term prognosis, reflecting residual left ventricular function after AMI.

Increased plasma adrenomedullin levels in patients with acute myocardial infarction in proportion to the clinical severity.

OBJECTIVES: To investigate the pathophysiological role of adrenomedullin in myocardial infarction. PATIENTS AND DESIGN: Plasma concentrations of adrenomedullin, atrial natriuretic factor, and brain natriuretic peptide were measured by radioimmunoassay in 31 patients with acute myocardial infarction over four weeks, and in 44 normal subjects. RESULTS: In patients with acute myocardial infarction, plasma adrenomedullin reached a peak of (mean (SD) 14.0 (9.0) pmol/l at 24 hours after the onset of symptoms and remained increased at all sampling points except the four week point compared with the value in normal subjects (5.0 (2.0) pmol/l). Adrenomedullin concentrations on admission were higher in patients from Killip class II, III, and IV than class I, and correlated positively with peak plasma creatine kinase and left ventricular end diastolic volume index, and negatively with left ventricular ejection fraction. The values from 12 to 48 hours were negatively correlated with systemic vascular resistance index. During the time course studied, adrenomedullin concentrations were positively correlated with atrial natriuretic factor (r = 0.40, p < 0.001) and brain natriuretic peptide (r = 0.53, p < 0.001). CONCLUSIONS: Plasma adrenomedullin concentrations increased in the acute phase of myocardial infarction in proportion with clinical severity suggesting that adrenomedullin may play an important role in the pathophysiology of myocardial infarction.

Esophageal perforation associated with profound shock successfully managed with hemodynamic assistance using percutaneous cardiopulmonary support.

A 51-year-old man was admitted to our hospital with complaints of severe chest pain, nausea, and vomiting. These symptoms had progressed rapidly and he was in shock. It was necessary to make a correct diagnosis as early as possible. However, the hemodynamic condition of the patient deteriorated rapidly before a definitive diagnosis could be established in spite of conventional therapies. Under hemodynamic assistance with percutaneous cardiopulmonary support (PCPS), a final diagnosis of esophageal perforation was made by esophagography. Our report illustrates a new application of PCPS for highly selected cases of noncardiogenic shock as a "bridge" until an accurate diagnosis is made and a specific treatment is applied.

[False aneurysm formation during the chronic phase of myocardial infarction at the margin of a previously-detected true aneurysm].

The patient was a 59-year-old man who had acute extensive anterior myocardial infarction in October, 1989. One month later, he was transferred to Kyoto University Hospital and underwent cardiac catheterization. Left ventricular aneurysm and significant stenosis in the proximal portion of the left anterior descending artery were documented. Because he experienced chest pain on slight exertion accompanied by a slight increase in the depth of the negative T wave on electrocardiogram, percutaneous transluminal coronary angioplasty (PTCA) was performed. Thereafter, chest pain disappeared, and the patient was discharged. Three months later, he was re-admitted to Kyoto University Hospital for a repeat cardiac catheterization after PTCA. PTCA site was found to be restenosed, and a small diverticulous aneurysm was found at the margin of the previously-detected ventricular aneurysm. As the diverticulous aneurysm was considered likely to precipitate the ventricular aneurysm into rupture, expeditious left ventricular aneurysmectomy was performed to prevent cardiac rupture. Ventricular aneurysms, common complications in myocardial infarction, are of two types, either true or false. Most aneurysms develop during the acute phase of myocardial infarction, and rupture of true aneurysms during the chronic phase of myocardial infarction rarely occurs. However, in the present case, a small diverticulous aneurysm, which was not demonstrated at the initial cardiac catheterization, developed during the chronic phase of myocardial infarction. Pathological examination revealed that the diverticulous aneurysm was a false aneurysm due to incomplete rupture. When the common pathogenesis of ventricular aneurysms in myocardial infarction is considered, the present report might represent an extraordinary rare case.(ABSTRACT TRUNCATED AT 250 WORDS)

Transition from compensatory hypertrophy to dilated, failing left ventricles in Dahl salt-sensitive rats.

To establish an experimental model for studying a specific transitional stage for compensatory hypertrophy to heart failure, we studied the pathophysiology of the left ventricle (LV) in Dahl salt-sensitive (DS) rats fed a high-salt diet. DS rats fed an 8% NaCl diet after the age of 6 wk developed concentric LV hypertrophy at 11 wk, followed by marked LV dilatation at 15-20 wk. During the latter stage, the DS rats showed labored respiration with LV global hypokinesis. All the DS rats died within 1 wk by massive pulmonary congestion. The dissected left ventricles revealed chamber dilatation and a marked increase in mass without myocardial necrosis. In contrast, corresponding Dahl salt-resistant (DR) rats fed the same diet showed neither mortality nor any of these pathological changes. The in vivo LV end-systolic pressure-volume relationship shifted to the right with a less steep slope in the failing DS rats compared with that in age-matched DR rats. Isometric contractions of LV papillary muscles isolated from these DS rats showed reduced tension development in the failing stage, but normal tension development in the hypertrophied stage. In conclusion, the DS rat fed a high-salt diet is a useful model showing rapidly developing congestive heart failure, in which the transition from compensatory hypertrophy to decompensatory dilatation of LV is easily and consistently manifested.

An asymmetric slice profile: spatial alteration of flow signal response in 3D time-of-flight NMR angiography.

We introduce an asymmetric slice profile technique, which alters the spatial response of the flow signal in 3D time-of-flight NMR angiography. By gradually increasing the flip angle from the inflow to the outflow portions of the slab, the inflow refreshment effect is distributed over a wide slab thickness. The asymmetric slice profile is simply produced by using a Gaussian RF excitation with an overlapping presaturation. The spatial distribution of steady flow signal in a phantom study demonstrated an essential agreement with a numerical simulation. 3D time-of-flight NMR angiography of volunteers' heads using this technique provided a smooth vascular depiction over a wide slab thickness.

Mechanism of the negative force-frequency relationship in physiologically intact rat ventricular myocardium--studies by intracellular Ca2+ monitor with indo-1 and by 31P-nuclear magnetic resonance spectroscopy.

We studied the subcellular mechanisms of the negative force-frequency relationship in rat myocardium by measuring 1) intracellular Ca2+ transients by indo-1 fluorometry and 2) intracellular pH (pHi) and phosphate compounds with 31P-nuclear magnetic resonance (NMR). The data were compared with those from guinea pig hearts, which show a positive force-frequency relationship. By increasing the pacing rate from 3 Hz to 5 Hz, the peak positive first derivative of left ventricular pressure (LVdP/dt) in rat heart decreased by 10 +/- 1% (n = 6). In contrast to this negative inotropic response, simultaneously measured peak Ca2+ transients increased by 6 +/- 1%. Guinea pig heart (n = 6) showed an increase in peak positive LVdP/dt (33 +/- 1%) which was associated with an increase in peak Ca2+ transients (8 +/- 1%). Under equivalent experimental conditions in an NMR spectrometer, this increase in the pacing rate did not affect intracellular levels of phosphate compounds in either rat (n = 6) or guinea pig heart (n = 6). In contrast, pHi showed a decrease of 0.031 +/- 0.006 pH units in rat heart, while no changes were observed in guinea pig heart. These results suggest that in physiological rat myocardium, pHi is susceptible to changes in the stimulus frequency and may affect the Ca(2+)-responsiveness of contractile proteins, which results in the negative force-frequency relationship.

Percutaneous transluminal coronary angioplasty of chronic total occlusions. Determinants of primary success and long-term clinical outcome.

This study was conducted to assess the determinants of the procedural success and long-term clinical benefits of percutaneous transluminal balloon angioplasty (PTCA) of chronic total occlusion (CTO) in recent years. Two hundred and twenty-six consecutive patients who underwent PTCA of CTO were divided into two groups according to the procedural success (n = 134) or failure (n = 92). Both groups were analyzed in terms of the initial success, predictors of procedural failure, and clinical outcome. The procedural success rate was noted to have improved to more than 70% since 1995. A multiple logistic regression analysis revealed that the presence of calcification, the length of the occlusion and the presence of multivessel disease were independent predictors of procedural failure. Cardiac death and the need for coronary surgery were significantly less frequent in patients with procedural success than in those with procedural failure. In properly selected cases, the success rate of PTCA of CTO is acceptable. Long-term clinical benefit is suggested by the high rate of freedom from coronary surgery and the low cardiac death rate in the patients who underwent successful revascularization.

Refractory coronary spasm relieved by intracoronary administration of nicorandil.

Two patients in whom coronary spasm was refractory to intracoronary injection of nitroglycerin were relieved by intracoronary administration of nicorandil (a nitrate and potassium channel opener) during catheterization. These findings suggest that nicorandil may prove useful as an additional therapeutic agent.

A randomised controlled trial of Prostar Plus for haemostasis in patients after coronary angioplasty.

OBJECTIVES: to clarify the efficacy and safety of Prostar Plus, a new percutaneous vascular surgical device (PVS) for vascular haemostasis. DESIGN: prospective randomised controlled trial. METHODS: a consecutive series of 60 patients were randomised to either PVS (n =30) or conventional manual compression ( n =30) following coronary angioplasty or stenting with femoral access using an 8-F sheath. RESULTS: PVS significantly shortened the time to haemostasis (10 s.d. 3 vs. 27 s.d. 9 min, p <0.001), ambulation (2.2 s.d. 0.9 vs. 11.0 s.d. 1.4 h, p <0.001), and discharge (2.2 s.d. 0.4 vs. 3.1 s.d. 0.7 days, p <0.01), compared with the manual compression group with no major complications. PVS also increased patient comfort assessed by using a visual-analogue scale method. Although these clinical benefits reduced the hospital cost ($1301 s. d. 248 vs. 1613 s.d. 460, p <0.05), the cost of the PVS device (approximately $350) cancelled the cost-saving benefit. CONCLUSIONS: this randomised study indicates that Prostar Plus is safe, more effective and comfortable than conventional manual compression.

Role of cytokines and adhesion molecules in ischemia and reperfusion in patients with acute myocardial infarction.

Although acute myocardial infarction (AMI) may involve both plaque rupture and ischemia-reperfusion injury, the pathogenesis of these phenomena is unclear. To elucidate the pathogenesis of AMI, serial measurements of platelet activating factor (PAF), interleukin-6 and cell adhesion molecules were made in patients with AMI. The PAF levels were measured upon hospital admission and at 24 and 72h in 8 patients with AMI. Serum levels of interleukin-6, soluble E-selectin (sE-selectin), soluble intercellular adhesion molecule-1 and soluble vascular cell adhesion molecule- 1 (sVCAM- 1) were measured upon admission and at 24 h and 4 weeks in 30 patients with AMI and 15 patients with stable effort angina. PAF levels were higher in patients with AMI than in normal volunteers; the increased levels lasting at least 72h. In contrast, interleukin-6 increased at 24h. sE-selectin was elevated at admission and sVCAM-1 increased later. sE-selectin levels upon admission in patients with additional ST-segment elevation after reperfusion were significantly higher than those in patients without ST-elevation. In patients with AMI, the time-course of changes in blood levels of cytokines varied according to the individual substances. Although it is unclear what is the precise role of each of the cytokines in the pathophysiology of AMI, sE-selectin may be possibly related to the reperfusion injury in the infarcted myocardium.

Survival using percutaneous cardiopulmonary support after acute myocardial infarction due to occlusion of the left main coronary artery--a report of two cases.

Two cases of acute myocardial infarction due to an occlusion of the left main coronary artery (LMCA) are presented. Their cardiogenic shock was successfully treated with percutaneous cardiopulmonary support (PCPS), in addition to reperfusion therapy and an intraaortic balloon pump. The 2 patients were able to be weaned from PCPS and discharged from hospital. It is suggested that the early use of PCPS may be life-saving in patients with myocardial infarction due to the occlusion of the LMCA who have progressed to cardiogenic shock.

Does coronary artery morphology predict favorable results of intracoronary thrombolysis in patients with unstable angina pectoris?

The efficacy of intracoronary thrombolysis (ICT) for unstable angina pectoris (UAP) has been limited, despite the similar pathogenesis between UAP and acute myocardial infarction. To ascertain the subset of UAP suitable for ICT, the clinical responses to ICT were assessed in patients with UAP. Eighty-2 patients with medically refractory angina were divided into 2 groups according to the coronary artery morphology of the culprit lesion before ICT: (1) lesions with acute cut off and/or filling defects (AC) and (2) lesions with a tapered shape (TA). The TIMI flow grade was determined from coronary angiograms before and immediately after ICT. The diameter stenosis (%DS) and minimal lumen diameter (MLD) of the culprit lesion were determined using quantitative coronary angiographic analysis before and immediately after ICT. In addition, inhospital cardiac event rates including urgent/emergency coronary angioplasty or bypass surgery, nonfatal myocardial infarction or cardiac death were compared between the 2 groups. Multivariate logistic regression analysis was performed using 13 clinical factors contributing to successful ICT. The results showed that all 3 coronary angiographic parameters (TIMI flow, %DS, and MLD) significantly improved in the AC group (p<0.01, p<0.01 and p<0.05, respectively), whereas none of these parameters improved in the TA group. The inhospital cardiac event rate after ICT was significantly higher in the TA group (76%) than in the AC group (48%; p=0.016). Odds ratio predicting successful ICT was 7.09 (p<0.01) for the AC lesion, and 2.54 (p<0.01) for new angina. In conclusion the AC lesions are more commonly associated with coronary thrombosis that responds to ICT than are the TA lesions. Thus, the coronary angiographic morphology may be an important predictor for a successful ICT in patients with medically refractory UAP.