We measured regional myocardial blood flow (RMBF) by positron emission tomography (PET) with ¹³N-ammonia at rest and during low-grade exercise using a bicycle ergometer fixed at 25 watts for 6.5 min. The ischemic area with severe coronary artery stenosis was evaluated in terms of quantitative RMBF. The study was performed in 46 subjects consisting of 19 patients with old myocardial infarction, 20 with effort angina pectoris, and 7 normal individuals. RMBF was calculated using the radioactivity in myocardial tissue measured by PET and the radioactivity in arterial blood. The PET data were compared with coronary arteriographic findings and ECG findings. When the analysis was restricted to the anterior wall of the myocardium, it was found that exercise caused RMBF to increase by 44.9% (n=28) in normal area, to increase by 23.3% (n=37) in severely stenotic area (stenosis≥90%), and to decrease by 17.4% (n = 20) in infarcted area. When we considered only the infarcted area of the entire heart, exercise caused RMBF to decrease by 26.6% (n=30) in the area of angiographically positive collaterals, and to increase by 0.8% (n=31) in the area of negative collaterals. Thus, we were able to quantitate the degree of ischemia in myocardium that was associated with severe coronary artery stenosis. By application of low-grade exercise, RMBF in normal myocardium increased, while RMBF in myocardium perfused by collaterals decreased.

View full abstract

Radiofrequency current catheter ablation was attempted for 17 morphologies of ventricular tachycardia (VT) in 14 patients. Five patients had underlying heart disease. The site of VT origin was determined as the earliest site of ventricular activation, or by pacing within the area of slow conduction. In 15 VTs, ablation was performed during VT, and 12 VTs (80%) were terminated within an average of 5.4±4.2 seconds. After ablation, 14 VTs (14/17=82%) of 11 patients (11/14=79%) could not be induced by electrical stimulation. Radiofrequency ablation appeared to be more effective in VTs without underlying heart disease (91%), and in VTs originating from the right ventricle (100%). Successful ablation sites usually showed a normal local electrograms during VT. Ablation in the slow conduction area was attempted in 3 VTs, and 2 VTs became noninducible. The mean number of applications of radiofrequency current for each VT origin was 7.7±6.4 at 20-50 Watts. In 4 patients, application of radiofrequency current was required 10 or more times because of a possible large arrhythmogenic area, or because of reinduction of VT, even though VT was terminated by radiofrequency current. No major complication was observed except for complete right bundle branch block in 1 patient. In conclusion: (1) Radiofrequency catheter ablation was considered to be effective and safe, especially for VT without underlying heart disease or VT originating from the right ventricle. (2) Ablation during VT was considered to be useful for identifying the proper ablation site and to avoid creating an unnecessary lesion.

View full abstract

Influence of arotinolol hydrochloride and atenolol on the balance between the sympathetic and parasympathetic nervous systems was evaluated in 8 hypertensive subjects by spectral analysis of heart rate (HR) and systemic blood pressure (BP). Before and after administration of either arotinolol (n=7) or atenolol (n=7) for 2 weeks, BP was continuously and non-invasively monitored by a finger-cuff manometry (Finapres) . A time series of instantaneous HR was constructed from the BP signal. A time series of mean BP was also constructed. Spectral analysis was performed by the use of an autoregressive algorithm on these time series (∼180 sec). Each spectrum was subdivided into low-(0.05-0.15 Hz, LF) and high-frequency (0.15-0.4 Hz, HF) components, and each component was divided by the sum of the two for normalization. As a measure of the balance between the sympathetic and parasympathetic nervous systems, the ratio of LF to HF (LF/HF) was evaluated. Arotinolol increased fractional HF in the HR spectrum from 0.45±0.12 to 0.73±0.08 (p<0.01) and decreased fractional LF from 0.55±0.12 to 0.27±0.08 (p<0.01); consequently, it decreased LF/HF from 1.4±0.5 to 0.4±0.2 (p<0.01). Atenolol had similar effects on these parameters. Neither of these β-adrenergic blockades produced a discernible decrease in LF/HF in the BP spectrum. In conclusion, these β -adrenergic blockades decreased LF/HF in the HR spectrum in hypertensive subjects, which suggests that they improved the balance between the sympathetic and parasympathetic nervous systems.

View full abstract

We compared the effects of 2 inotropic agents, dobutamine and isoproterenol, on regional coronary blood flow, contractile function, hemodynamics and levels of phosphate compounds in the acutely ischemic canine heart. Dogs were instrumented to determine regional coronary blood flow (non-radioactive microsphere method), contractile function (sonomicrometry), and hemodynamics. Myocardial phosphate compounds were measured simultaneously by the phosphate-31 (³¹P) magnetic resonance spectroscopic technique. Both drugs augmented the global performance of the heart, but produced no significant improvement in regional contractile function in the ischemic region. Isoproterenol significantly increased the ratio of inorganic phosphate to phosphocreatine in the ischemic region, as compared to dobutamine. However, no significant differences were seen in myocardial lactate consumption with inotropic stimulation between the 2 groups. ³¹P magnetic resonance spectroscopy could be used to differentiate between the effects of dobutamine and isoproterenol on energy metabolism in ischemic myocardium despite the lack of significant differences in regional function and myocardial lactate consumption. The significant tachycardia without an augmentation of systemic blood pressure induced by isoproterenol may account for this unfavorable effect on myocardial energy metabolism.

View full abstract

To determine the optimal temperature for catheter heat mapping without damaging cardiac tissue, we studied the electrophysiologic and histologic responses of the atrioventricular (AV) conduction system exposed to a specific range of temperatures. In 18 closed-chest dogs, an electrode catheter with a thermistor, tip was positioned transvenously at the AV junction. Radiofrequency current (RFC) was applied in incremental temperature steps until transient 2nd-degree AV block was induced. Catheter tip temperature (CTT) was measured at each step. RFC was immediately discontinued when AV block occurred. AV conduction was evaluated before and 4 weeks after the procedure. Acute transient 2nd-degree AV block was induced in 45 applications, during which the average CTT was 48.7±2.7°C. In another 40 applications in which 2nd degree AV block was not induced, the average CTT was significantly lower [46.3±2.5°C] (p<0.001). Eleven of 16 dogs showed acute 2nd-degree AV block, but had normal AV conduction at 4 weeks (Group A). In the other 5 dogs, 1st-degree AV block was seen at 4 weeks (Group B). The lowest CTTs in Groups A and B were 45 and 49°C, respectively. Histologic findings in 2 dogs from Group A revealed that 10-15% (by area) of the AV node was fibrotic. These findings suggest that the induction of fully reversible AV block can be achieved by titration of RFC, during the application of RFC to the AV junction. In conclusion, RF energy was used to produce a tip temperature of between 45°C and 49°C, which induced reversible and significant interruption of conduction of in tissue in the AV junction, and presumably also in target sites in clinical RF ablation.

View full abstract

Angiotensin II is well known to have a cardiotoxic effects. However, it is still unclear whether exogenous angiotensin I or angiotensin II has a deleterious effect on myocardial ischemia-reperfusion injury. To examine this deleterious effect, we administered angiotensin I and angiotensin II to perfused hearts before ischemia, and measured creatine kinase (CK) release and cardiac function during subsequent reperfusion. Wistar Kyoto rats were used and the hearts were perfused by the Langendorff technique at a constant flow (10 ml/min). Seven hearts were perfused for 20 min and then subjected to 15 min of global ischemia (Control). In the experimental groups, during the 5 min before ischemia, we administered 100 ng /ml angiotensin I (Ang I; n=9), 1 μg/ml enalaprilat (ACEI; n=5), both agents (ACEI+Ang I) (n=6), or 10 ng/ml angiotensin II (Ang II; n = 6) . The perfusates were then sampled to measure angiotensin II. After 15 min of ischemia, the hearts were reperfused with control perfusate. Throughout the 20 min of reperfusion, the effluent was collected to measure cumulative CK release. Angiotensin I increased coronary perfusion pressure (CPP) by 32±4 mmHg, however, the angiotension converting enzyme inhibitor inhibited the increase of CPP by angiotension I (11±1 mmHg) (p<0.01). The contents of angiotensin II in the effluent in Ang I and Ang I+ACEI were 11.5±1.9 ng/ml and 4.0±0.5 ng/ml (p<0.01). After 20 min of reperfusion, the left ventricular developed pressure was unchanged in all of the groups. CPP was also unchanged by ischemia in all of the groups. Ventricular fibrillation was occurred only in Ang I and Ang II, with an incidence of 44% and 33%, respectively. The cumulative CK in Control, Ang I, ACEI, Ang I+ACEI, and Ang II was 7±1 IU, 19±2 IU, ** 7±1 IU, 12±1 IU⁺ and 20±2** IU. (**; p<0.01 vs Control.⁺ ; p<0.05 vs Ang I). Angiotensin I (100 ng/ml) and angiotensin II (10 ng/ml) both produced ischemia-reperfusion injuries. Angiotensin I is converted to angiotensin II in cardiac tissue, and this angiotensin II is supposed to have a deleterious effect on ischemia-reperfusion injury. This harmful effect may not be related to the vasoconstriction induced by angiotensin II.

View full abstract

A 38-year-old man (Case 1) suddenly collapsed while resting. His 54-year-old brother (Case 2) came soon thereafter began to perform cardiac massage and mouth-to-mouth resuscitation. However, the elder brother suddenly died after resuscitating his younger brother for about 30 minutes. Necropsy revealed an occlusive thrombus of the left anterior descending coronary artery and coagulation necrosis of the myocardium in Case 1. Case 2 was diagnosed as sudden cardiac death on the basis of the moderate coronary sclerosis and myocardial lesions including contraction band, fragmentation, waviness, bleeding, and mild subendocardial fibrosis. Pulmonary edema in the both cases revealed the presence of left ventricular heart failure. Case 2 is a good example of the contribution of psychological and physical stress to sudden cardiac death.

View full abstract

We report a patient who experienced a reversible prolongation of the QT interval and episodes of syncope while receiving probucol. A 64-year-old woman experienced syncopal attacks 8 and 11 weeks after beginning probucol treatment (500 mg twice daily) . The pre-treatment ECG showed a slight prolongation of the corrected QT interval (QTc) (0.46 sec). Her QTc increased to 0.62 sec 12 weeks after beginning probucol treatment and decreased to about the baseline value (0.48 sec) 6 weeks after treatment was discontinued. Probucol is known to prolong the QT interval. A long QT interval has been linked to an increased risk of ventricular arrhythmias, syncope or sudden death. However, clinical reports which causally relate probucol treatment to syncope are very rare. Although an ECG during the episodes of syncope was not available, this patient's syncope might be due to ventricular tachyarrhythmia associated with probucol-induced QT prolongation. This case emphasizes the need for careful evaluation of the QT interval before and during probucol treatment.

View full abstract