Myocardial perfusion abnormalities occur in the absence of epicardial coronary artery disease in patients with a wide spectrum of cardiovascular disorders including microvascular angina, hypertension and left ventricular hypertrophy, coronary atherosclerosis, hypercholesterolemia, and non-ischemic left ventricular dysfunction. These patients have limited coronary microvascular dilator reserve which occasionally is associated with evidence of myocardial ischemia. Primary microvascular hyperconstriction (spasm) is also proposed to cause myocardial ischemia in a subset of patients with rest angina. There is ample evidence suggesting that endothelial dysfunction contributes to microvascular dysfunction, but the precise mechanism of endothelial dysfunction is not known. Nitric oxide is one of the key molecules which control microvascular tone and therefore coronary blood flow, and its decreased availability appears to be involved under certain conditions. This hypothesis has attracted considerable interest as a new therapeutic strategy for these patients having coronary microvascular derangements caused by divergent cardiovascular diseases.

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The purpose of this study was to evaluate the rupture and dissection of the vessel wall immediately after balloon dilatation by intravascular ultrasound (IVUS) imaging and to predict restenosis in patients who underwent subsequent coronary stent implantation. Stent implantation improves the long-term results of coronary angioplasty by reducing lesion elastic recoil and arterial remodeling. However, serveral studies have suggested that neointimal hyperplasia is the cause of in-stent restenosis. We recruited 60 patients in whom IVUS studies were performed immediately after successful balloon dilatation and just before stent implantation. We compared IVUS parameters with 6-month follow-up quantitative coronary angiography. This was performed in 51 lesions of 51 patients (85%). Qualitative analysis included assessment of plaque composition, plaque eccentricity, plaque fracture and the presence of dissection. In addition, minimal luminal diameter, percent diameter stenosis, percent area stenosis and plaque burden were quantitatively analyzed. Two morphological patterns after balloon dilatation were classified by IVUS. Type I was defined as absence or partial tear of the plaque without disclosure of the media to lumen (22 lesions). Type II was defined as a split in the plaque or dissection of the vessel wall with disclosure of the media to the lumen (29 lesions). At 6 months follow-up, angiographic restenosis occurred in 17 of the 51 lesions (33%). Restenosis was significantly (p < 0.05) more likely to occur in type II (13/29: 45% incidence) than in type I (4/22: 18% incidence). The assessment of plaque morphology immediately after balloon dilatation and before stent implantation provides important therapeutic and prognostic implications.

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The difference between the maximum and minimum QT intervals on the standard 12-lead ECG (QT dispersion) may be a significant predictor of serious arrhythmias. Dynamic changes in QTd were determined during exercise-induced ischemia in 15 patients with effort angina (≥75% coronary stenosis) and 10 normal individuals. Treadmill exercise testing was performed according to Bruce's protocol and the rate-corrected QT dispersion (QTcd) was calculated using Bazett's formula. The resting QTcd before exercise was similar in the angina patients and the controls. After the first stage of exercise, QTcd was significantly increased in the angina patients (p=0.035), while it remained near baseline in the controls. Five minutes after completing exercise, QTcd was significantly greater in the angina patients than in the controls (p=0.011). Furthermore, QTcd values after the first stage of exercise were significantly correlated with the maximum ST depression observed on completing exercise in the angina patients (r=0.714, p=0.0028). Because QTd may represent the heterogeneity of ventricular repolarization, its significant exercise-induced increase in the angina patients suggests that myocardial ischemia caused repolarization disorders. The significant correlation between QTcd values after the first stage of exercise (before significant ST depression) and the maximum ST depression on completing exercise suggests that an increase in QTcd proceding ischemic ST depression may predict myocardial ischemia. In addition, even daily activities not causing significant ST changes may increase QTcd and the risk of serious arrhythmia in angina patients.

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The aim of the present study was to evaluate the relationship between exercise capacity and ventilatory response in patients with stable old myocardial infarction. We performed cardiopulmonary exercise test in 61 patients with stable old myocardial infarction and in 30 healthy men. Each subject exercised on a bicycle ergometer until exhaustion. Patients who had anginal pain or electrocardiographic ischemic changes during exercise were excluded. The patients were classified into three groups according to peakVO₂ achieved during exercise, using Weber's method: group A, peakVO₂≥21 ml/min/kg (n=4); group B, 14≤peakVO₂<21 ml/min/kg (n=45); and group C, peakVO₂<14 ml/min/kg (n=12). With progressive increases in VCO₂, VE increased linearly below the anaerobic threshold (AT) level. The slope of the linear regression line between VCO₂ and VE (SLOPE) was calculated in each subject. The mean SLOPE of the healthy men (group N) and groups A, B and C were 25.8±0.5, 25.1±0.5, 28.9±0.8 and 37.1±1.7 (×10^-3), respectively. Thus, the SLOPE was steeper in patients with lower peakVO₂. It is difficult to perform a maximal exercise tolerance test on patients with chronic heart failure to evaluate their exercise capacity. We can assess exercise capacity by the slope of the linear regression line between VCO₂ and VE (SLOPE) at the lower exercise level.

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Ventricular premature contractions (VPCs) occasionally appear successively in the form of bigeminy, trigeminy or quadrigeminy associated with quiescent periods. However, details of these rhythmic VPC bursts have not been well documented. We analyzed the incidence, periodicity and interval of VPC bursts exhibiting bigeminy or trigeminy using ambulatory ECG monitoring and computer analysis. We defined VPC bursts as more than 5 successive groups of VPCs each containing more than 20 VPCs in the form of bigeminy or trigeminy that were interrupted by normal sinus rhythm lasting for more than 60 seconds. Bursts thus defined were observed transiently or continuously in 78 out of 500 consecutive patients showing > 3000 VPCs a day. Their age ranged from 14 to 76 years (mean 48). Forty patients were men and 38 were women. We could discriminate between two types of bursts on the instantaneous heart rate tachograms. Dome type bursts(n=48) showed gradual shortening of the VPC coupling intervals whereas horizontal type bursts (n=30) demonstrated fixed coupling intervals during the bursts. Cycle length of the dome type burst was 185 ± 40 seconds and regular, whereas it was 210 ± 63 seconds and irregular in the horizontal type (NS). Duration of the VPC bursts was 101 ± 31 seconds in the dome type and 98 ± 41 seconds in the horizontal type. Both burst types were associated with transient increases in sinus rate and abbreviated VPC-VPC intervals. We suspect ventricular parasystole to be the mechanism of these bursts especially in the dome type. Recognition of these two burst types from heart rate tachograms may be of value in the suppression of VPCs.

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Although the effects of right ventricular (RV) volume and pressure overload (RVVO and RVPO) on ventricular septal motion are different, the differential effect on left ventricular (LV) function is still controversial. The Doppler-derived index (Tei index) combining systolic and diastolic ventricular function, defined as the sum of isovolumetric contraction time (ICT) and isovolumetric relaxation time (IRT) divided by ejection time (ET), has been demonstrated to be a useful index to estimate LV function and to predict the prognosis of patients with congestive heart failure. This study was designed to evaluate the differential effects of RVVO and RVPO on LV function using the Tei index. Study patients consisted of 26 age-matched normal subjects, 22 patients with atrial septal defect (ASD) with normal or borderline RV pressure and 25 with primary pulmonary hypertension (PPH). All subjects had normal LV ejection fractions measured with 2-dimensional echocardiogram using biplane Simpson's method (61 ± 4 vs 61 ± 4 vs 63 ± 8 %, normal vs ASD vs PPH). Tei index was easily obtained in all subjects from transthoracic Doppler echocardiogram of LV inflow and outflow. Patients with ASD had normal ICT, IRT and ET, resulting in normal Tei index, however, patients with PPH had significantly prolonged ICT and IRT with shortened ET, resulting in a significant increase in Tei index (0.38 ± 0.04 vs 0.36 ± 0.03 vs 0.61 ± 0.22, p < 0.001). Although RVVO due to ASD has no significant effects on LV function, RVPO due to PPH can adversely affect LV function. The Tei index is a simple and sensitive measure to assess LV function caused by RVVO or RVPO.

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We studied the distinctive morphology of the left ventricle (LV) and attempted to relate advanced age and hypertension to this characteristic feature in elderly patients with hypertrophic cardiomyopathy (HC). Fourteen elderly patients ≥ 85 years old (mean age 90 ± 5 years) with HC were compared with 45 young patients ≤ 40 years (mean age 34 ± 4 years) with this disease. More mild hypertension in the elderly (10/14, 71%) than in the young (0%), and more syncope in the young (10/45, 22%) than in the elderly (0%) were observed. Echocardiography showed that the elderly patients had relatively mild LV wall thickening, generally confined to the septum (elderly vs young: 18 ± 4 vs 25 ± 8 mm, p < 0.001), with more basal septal bulging (elderly vs young: 12/14, 86% vs 0%, p < 0.001) and anterior septal hypertrophy of LV (elderly vs young: 11/14, 79% vs 0%, p < 0.001). Elderly patients with mild hypertension showed a predominantly basal septal bulging (10/10, 100%) and anterior septal hypertrophy of LV (9/10, 90%). HC in elderly patients ≥ 85 years old has a striking LV morphology. Mild hypertension and advanced age may contribute to the distinctive geometry.

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We investigated the angiogenic and myocardial salvage effects of bFGF. Twelve beagles with ligated left anterior descending coronary arteries were divided into two groups: a FGF group administered bFGF intravenously, and a Control group, after CAG immediately post-ligation. One week post-ligation, CAG was repeated. The heart was sliced along the short axis. For each section, the fluorescein Na staining deficit area (DA) and ratio of DA to total area (DAR), TTC staining of the infarct area (IA) and ratio of IA to total area (IAR), and Masson trichrome staining of the fibrosed area (MA) and ratio of MA to total area (MAR), were calculated. The increase in the number of collateral vessels, seen on CAG from post-ligation to 1 week later, was significantly greater in the FGF group. No significant differences in IAR or MAR were seen between the groups. However, DAR and DA/IA were significantly less in the FGF group. In conclusion, bFGF had no effect on infarct size, but stimulated the growth of collateral vessels and improved coronary blood flow in IA.

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The purpose of this study was to establish an animal model in which ventricular fibrillation (VF) can be induced reproducibly and defibrillation can be accomplished repeatedly. The left anterior descending artery (LAD) was cannulated and perfused with blood from the carotid artery in eleven openchest dogs. Electrodes of the internal defibrillator were inserted in the cavities of the left atrium and left ventricle via incisions in the left atrial appendage and left ventricular apex. The perfused blood temperature was modulated to produce regional myocardial warming (42°C) or cooling (28°C). In all dogs, VF was repeatedly induced by the combination of warming and left ventricular extrastimuli and by the combination of cooling and right ventricular extrastimuli. The VF was quickly defibrillated by use of the internal defibrillator. The mechanism of VF was found to be reentry by the analysis of activation sequences. This VF model may be useful when evaluating the efficacy of antiarrhythmic drugs because of the high reproducibility.

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We studied a new technique for creating long linear lesions in hearts using a custom-made linear probe. Radiofrequency (RF) energy applications using a 25-mm long stainless steel linear probe and a corresponding 500-kHz energy generator were tested, creating 90 lesions in isolated porcine hearts. The RF current was applied between the linear probe and a large patch electrode attached to the back of the specimen. Three parameters, comprising the power of the delivered energy, the pressure of contact between the probe and the specimen, and the duration of energy delivery were changed independently and the size of the resulting lesions was measured. All 90 lesions were transmural, well demarcated and created by a single stationary RF application. Lesion length and width increased with: 1) increasing power, when the other two parameters were maintained at constant levels, 2) increasing contact pressure, when the other two parameters were maintained at constant levels, and 3) increasing duration of energy delivery when the other two paramaters were maintained at constant levels. The maximum width of the lesions was 3.7 mm. No overheating of any of the specimens was observed. In conclusion, the new original long linear probe used in this study was effective for creating transmural linear lesions, presenting the possibility of a worthwhile contribution to the maze surgical procedure applied to atrial fibrillation.

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A cDNA of a tentative A-kinase anchoring protein, presumably coupled with heterotrimeric GTP binding protein α 13 subunit (G α 13), was cloned from a human heart cDNA library. It was approximately 650 bases and its mRNA was expressed in the heart. Homology search of DNA sequences revealed that it was a novel cDNA with 84% homology with the partial sequence of rabbit cDNA of AKAP 120 without a stop codon. 3'-Rapid Amplification of cDNA Ends (3'-RACE) and yeast functional assay were performed to determine the 3'-end of the cDNA and ribosomal frameshifting was suggested as a translational mechanism. Here we report that a protein encoded by the cDNA may be involved in intracellular signal transduction via the G α 13 and PKA in hearts.

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To investigate the relationships between the activity in potential operated Ca²⁺ channels (POC), blood pressure, and endothelium in hypertension, we tested the contractile responses to a Ca²⁺ channel agonist Bay K 8644 (BAY K) in aorta from deoxycorticosterone-acetate-saline (DOCA-S) and reduced renal mass-saline (RRM-S) hypertensive rats. The effects of mechanical rubbing, Nω-Nitro-L-Arginine Methyl Ester (l-NAME) and indomethacin were also examined. Sensitivity to BAY K increased in experimental rats before they became hypertensive and contractile responses were enhanced as hypertension developed. Force development to BAY K was correlated with blood pressure levels. Endothelium removal enhanced the contractile response to BAY K. L-NAME, but not indomethacin, potentiated the response to BAY K. Contractile response to BAY K was negatively correlated with relaxation to acetylcholine. An enhanced contractile response to BAY K was observed also in aged rats. Enhanced activation of vascular POC in hypertension results from elevated blood pressure and partly from diminished inhibitory action of endothelium. Senescence also enhances vascular POC activity.

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To examine the circadian and infradian rhythms of paroxysmal atrial fibrillation, the time and date of 85 arrhythmic attacks occurring over a period of 4 years were analyzed in a patient with reliable symptoms. In the hourly analysis, a remarkable circadian rhythm similar to the reported population circadian rhythm was observed. On a day basis, the distribution of the intervals between 2 successive episodes showed a significant departure from the exponential distribution, indicating the arrhythmia was not a simple probabilistic phenomenon. Spectrum analysis revealed a prominent peak occurring at about 0.3 cycles/day, suggesting a possible circasemiseptan rhythm. Thus, in this patient, paroxysmal atrial fibrillation was not a random event when observed not only from an hour incremental perspective but also from a day incremental perspective, suggesting the circadian and infradian rhythms of this arrhythmia.

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A clinicopathologic study was performed in a 77-year-old female with hypertrophic cardiomyopathy who had experienced recurrent syncopal attacks due to Torsades de Pointes (TdP) following QT prolongation and atrioventricular block. She died suddenly two years later while eating dinner. Pathologic findings of the heart showed a dilated and hypertrophied left ventricle. The heart weighed 550 g. There were two foci of localized endocardial fibroelastosis (EFE) beneath the aortic valve, one with a size of 3.5 × 3.5 cm, and the other (2 × 1 cm) located on the upper ventricular septum. Histologic findings showed hypertrophy and disarray in the left ventricular myocardium. The conduction system using serial sectioning revealed remarkable bilateral bundle branch fibrosis and hypertrophied Purkinje fibers in the left bundle branch adjacent to the EFE on the ventricular septum. These findings were thought to be related to the occurrence of TdP.

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Four cases of lower extremity hematoma in patients undergoing anticoagulant therapy after heart valve replacement are herein reported, with special emphasis on the comparative diagnostic value of ultrasonography and computerized tomography. Although conservative management is sufficient for patients with no neurological impairment, needle aspiration after autolysis of the hematoma, which can be confirmed by CT study, is also recommended.

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