To characterize abnormalities in pulmonary venous flow velocity patterns and to explore the changes in these patterns following short-term (3 to 14 days) administration of vasodilators, pulmonary venous and mitral flow velocity patterns were serially studied at congestive heart failure and after vasodilator administration in 18 patients. Peak mitral early diastolic filling velocity (E) and the ratio of E to peak filling velocity at atrial contraction (E/A) consistently decreased after vasodilator administration by 30±4 cm/s and 0.74±0.13 (mean ± SD), respectively. Peak pulmonary venous diastolic forward flow velocity also decreased by 29±4 cm/s. However, changes in peak pulmonary venous systolic forward flow velocity (S, cm/s) did not correlate with changes in E, the E/A ratio, or D (peak pulmonary venous diastolic forward flow velocity). Thus, when patients were divided into two groups on the basis of changes in S, indices of left ventricular systolic performance, such as end-systolic dimension and fractional shortening, improved more in the group which showed an increase in S after vasodilator administration than in the group which showed a decrease in S (-7±6 vs -1±4 mm, p<0.05; 8±6 vs -1±4%, p<0.05). Although the mitral flow velocity pattern changed uniformly with vasodilator administration in patients with mild to moderate congestive heart failure, the changes in pulmonary venous flow velocity patterns were not uniform among patients. Pulmonary venous flow velocity patterns appear to reflect changes in left ventricular systolic performance in addition to those in left ventricular diastolic performance.

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The relationships between plasma Lipoprotein(a) (Lp(a)) levels and plasminogen activator inhibitor (PAI) activity and tissue plasminogen activator (t-PA) antigen levels were studied in 15 patients with unstable angina. Plasma levels of Lp(a) (mg/dl) were significantly higher in patients with unstable angina after treatment 2 weeks than on admission (19.7±2.8 vs 14.6±2.3, p<0.01). On the other hand, the plasma levels of PAI activity (IU/ml) and t-PA antigen (ng/ml) in patients with unstable angina were significantly higher on admission than after treatment (PAI activity: 11.4±1.4 vs 7.7±1.5, t-PA antigen: 8.7±0.9 vs 7.0±0.9, p<0.01). We conclude that patients with unstable angina have re duced fibrinolytic capacity, as indicated by increased PAI activity, and that the plasma Lp(a) level may be decreased due to binding with fibrin during the acute stage of unstable angina.

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Acute changes in blood pressure and heart rate during cigarette smoking were investigated in 10 elderly subjects aged 75.6±4.8 (mean±SD) years and in 10 non-elderly subjects aged 35.6±10.5 years. All subjects were healthy normotensive men with no cardiovascular disease. While each subject smoked two cigarettes containing 5.4 mg of nicotine, systolic and diastolic blood pressures increased significantly more in the elderly subjects (18.2±6.0/9.0±5.0 mmHg) than in the non-elderly subjects (4.8±4.7/3.9±4.2 mmHg, p<0.05). However, the increases of heart rate in the two groups were similar (elderly: 10.5±4.1 beats/min versus non-elderly: 12.1±6.4 beats/min, ns). These results indicate that there is an age-related difference in blood pressure elevation during cigarette smoking in healthy subjects.

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We performed catheter ablation in 10 consecutive patients with idiopathic monomorphic right ventricular tachycardia and studied the long-term outcome. A11 ventricular tachycardias had a left bundle branch block configuration with an inferior axis, and originated from right ventricular outflow. Antiarrhythmic drugs (3-6 drugs) had been ineffective in controlling ventricular tachycardia. The 2 patients who underwent direct-current ablation (2 shocks of 150 J) had no recurrence of ventricular tachycardia and did not require antiarrhythmic drugs during a follow-up of 56 and 51 months, respectively. Of the 8 patients who underwent radiofrequency ablation (30-40 watt, 20-40 sec, 2-15 application, using Inter Nova RA 50, 13.56 MHz), I patient had no recurrence of ventricular tachycardias and did not require antiarrhythmic drugs, 4 patients had no recurrence of ventricular tachycardias but did require anti-arrhythmic drugs, and 3 patients experienced recurrence of non-sustained ventricular tachycardia despite the use of antiarrhythmic drugs during a follow-up of 15 -40 months. There were no complications except for cardiac perforation which occurred immediately after direct-current ablation in I patient. In conclusion, long-term success in preventing ventricular tachycardia was achievable with direct-current ablation, but this success was associated with serious risks, such as cardiac perforation. Radiofrequency ablation was safer than direct-current ablation, but had a lower long-term success rate.

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Myocardial ischemia interrupts neurotransmission and causes the depression of norepinephrine release. However, the effects of sympathetic nerve stimulation on neurotransmission and norepinephrine release in post-ischemic myocardium are not well defined. We measured regional myocardial length and nor-epinephrine (NE) release during sympathetic nerve stimulation in anesthetized dogs. Dogs were divided into 2 groups: Group I (n=14); sympathetic nerve stimulation, Group 2 (n=9); pre-treatment with α-blockade yohimbine hydrochloride (0.2 mg/kg) followed by sympathetic nerve stimulation. The left anterior descending artery was occluded for 15 min. Sympathetic nerve stimulation was performed before coronary occlusion and after reperfusion. In group 1, the decrease in systolic shortening in the ischemic region persisted for more than 60 min. Although sympathetic nerve stimulation caused an increase in systolic shortening, it was lower than the pre-ischemic value. NE release from the post-ischemic myocardium remained decreased for 60 min. The decrease in the post-ischemic myocardial response to sympathetic nerve stimulation was associated with diminished NE release. When the cardiac sympathetic nerve was denervated with an epicardial phenol application, NE release decreased even further. In group 2, NE release did not decrease following reperfusion. These results suggest that sympathetic nerve conduction is not completely impaired in post-ischemic myocardium and that pre-synaptic a -2 receptors might play an important role in diminished NE release.

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BMY21190, an inhibitor of cyclic AMP phosphodiesterase, has a coronary vasodilating effect. BMY21190 was evaluated for its ability to modify the development of experimental thrombosis resulting from anodal current injury (100 μA for 6 h) of the intimal surface of the left circumflex coronary artery (LCX) in anesthetized dogs. Two groups of dogs were studied. One group received BMY21190 (1 mg/kg) and the other group received an equal volume of vehicle infused into the left jugular vein. After a 30 min administration of BMY21190, heart rate and mean coronary blood flow were increased significantly and mean arterial pressure was decreased. However, the myocardial tension of the left anterior descending coronary artery (LAD) and LCX areas did not increase significantly after BMY21190 infusion. During LCX stimulation, the first LCX occlusion and hyperemic reaction of the control group both occurred significantly earlier than those of the BMY21190 group. BMY21190 treatment reduced the development of the LCX thrombus mass, as compared to that in the controls. In ex vivo studies, platelet aggregation in response to arachidonic acid, ADP or collagen was inhibited by BMY21190. These results suggest that BMY21190 possesses anti-thrombotic and coronary vasodilating effects which may be mediated through the inhibition of cyclic AMP phosphodiesterase.

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Recent studies have indicated that specific dihydropyridine-sensitive Ca²⁺ channel binding sites are present in the brain, and that they play a crucial role in synaptic function. The present study was performed to determine the effects of nicardipine, a dihydropyridine-sensitive Ca²⁺ channel blocker, on the release of acetylcholine in the rat central nervous system. Striatal slices of rats which had been prelabelled with [³H]acetylcholine were superfused with Krebs-Ringer solution. The slices were stimulated with either electrical pulses (1 Hz) or an excitatory amino acid, L-glutamate, and the effects of nicardipine on the release of acetylcholine were examined. Electrical stimulation produced an in-crease in [³H]acetylcholine release from the striatal slices. Exposure of the slices to nicardipine significantly inhibited the stimulation-evoked [3H] acetylcholine release. An endogenous excitatory amino acid, L-glutamate, also elicited release of [³H]acetylcholine. Nicardipine significantly reduced the L-glutamate-induced release of [³H]acetylcholine, and the effect was pronounced in the presence of Mg²⁺. These results demonstrate that nicardipine inhibits both electrically and chemically stimulated [³H]acetylcholine release from rat striatum. The ability of nicardipine to inhibit cholinergic transmission may be related to the central effect of this Ca²⁺ channel blocker.

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The purpose of this study was to compare vascular damage and thrombus formation in the coronary and femoral arteries after balloon angioplasty, and to develop a physiological animal model of intracoronary occlusive thrombus using the balloon angioplasty technique. Angioplasty of the left anterior descending coronary arteries of 14 dogs was performed with an oversized balloon catheter at a high inflation pressure (150 PSI). This was followed angiographically (PTCA protocol). Dogs that showed arterial occlusion were divided into 2 groups. The dogs in I group were killed with an overdose of sodium pentobarbital, and those in the other group were infused with a tissue-type plasminogen activator (t-PA; 300, 000 unit/kg). Angioplasty of the femoral and profunda femoris arteries (n=5) was performed in 5 other dogs (PTA protocol). All of the animals were eventually sacrificed and tissue preparations were made from all 3 types of arteries. In the PTCA protocol, acute arterial occlusion was seen angiographically within 2 h in 10 of the 14 dogs. A histological study of the acutely occluded arteries (n=5) showed thrombotic occlusion and severe arterial damage with medial tearing. T-PA was infused to 5 of the dogs with acute occlusion, and all showed reperfusion. A histological study of these animals showed severe arterial damage, but no macroscopic thrombus. In 4 dogs with-out acute occlusion, none of the 10 arteries examined were acutely occluded. In the PTA protocol, none of the 10 arteries were acutely occluded. A histological study showed fewer thrombi and less severe arterial damage. The media and adventitia of normal coronary arteries had less elastic fiber than the normal femoral and profunda femoris arteries. Differences in arterial structure can account for the differences in arterial damage and thrombus formation. Thus, oversize balloon angioplasty of canine coronary arteries frequently resulted in acute thrombotic occlusion. This method may be useful as an animal model of thrombosis.

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This study was undertaken to examine the effects of hydrogen peroxide on stimulatory guanine nucleotide-binding protein (Gs), and coupling in the β-aderenergic receptor - Gs - adenylate cyclase system in rat heart, in vitro. Cardiac membranes were preincubated with various concentrations (0.1, 1, and 10 mM) of hydrogen peroxide at 30°C for 5, 10, 30 and 60 min. Although the assay of β-adrenergic receptors involving [³H]-dihydroaloprenolol ([³H]-DHA) binding revealed that the maximal number of binding sites (B_max) was not altered, the dissociation constant (K_d) for [³H]-DHA was increased in the presence of I mM and 10 mM hydrogen peroxide (control 0.68±0.16 nM, vs 1 mM H202 1.13±0.16, 10 mM H202 1.01±0. 12). Conversely, no significant changes in Gs activities were observed in hydrogen peroxide-treated groups. Adenylate cyclase activity (stimulated by forskolin) was significantly reduced by 10 mM hydrogen peroxide after a 5 min preincubation period (control 277.1±19.2 pmol cAMP/mg protein/min, H202 230.3±14.9). The amounts of cyclic AMP produced by the stimulation of membranes with GTP, GTP + (1)-isoproterenol, guanylimidodiphosphate (Gpp(NH)p) or Gpp(NH)p+(1)-isoproterenol were significantly lower in 10 mM hydrogen peroxide-treated groups than those in controls (GTP: control 57.6±5.6pmol cAMP/mg protein/min vs H₂O₂ 46.4±6.9, GTP+(1)-isoproterenol: control 83.9±10.2 vs H₂O₂ 67.7±10.3, Gpp(NH)p: control 77.5±8.8 vs H₂O₂ 61.0±8.6. Gpp(NH)p+(1)-isoproterenol: control 105.0±13.1 vs H202 83.9±12.2, forskolin: control 223.2±13.8 vs H202 182.8±18.4). In the presence of hydrogen peroxide, the extents of the depression in cAMP production induced by GTP. GTP+isoproterenol, Gpp(NH)p, and Gpp(NH)p+ (1)-isoproterenol were similar to those induced by forskolin stimulation. These results indicate that hydrogen peroxide does not affect Gs activity or coupling in the p-receptor - Gs - adenylate cyclase system, but does depress CAMP production by inhibiting adenylate cyclase.

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We encountered a 67-year-old woman with a left atrial myxoma which was discovered during echocardiographic examination and emergency coronary arteriography just after an onset of acute inferior myocardial infarction. Coronary arteriography disclosed an abrupt and total occlusion of the right coronary artery and an abnormally large and tortuous atrial circumflex branch feeding a left atrial mass. These findings were the most useful for diagnosis. Aorto-coronary bypass surgery and excision of the myxoma were performed simultaneously by emergency operation. The postoperative course was uneventful. Myocardial infarction in this patient is believed to have been caused by coronary embolization from the left atrial myxoma.

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We present a 46-year-old male with unstable angina and bilateral coronary-to-pulmonary artery fistulae in whom reversible myocardial ischemia was detected by exercise-stress thallium-201 single-photon emission computed tomography (SPECT). Coronary angiography revealed a 99% stenosis at the proximal site of the left descending coronary artery and bilateral coronary-to-pulmonary artery fistulae with a saccular aneurysm. Percutaneous transluminal coronary angioplasty abolished chest pain and electrocardiographic changes. However, definitely improved, but still present, stress-induced perfusion abnormalities were demonstrated by an exercise-stress thallium-201 SPECT study. Myocardial ischemia was the only serious complication related to the coronary fistulae, and after they were surgically resected, the reversible perfusion abnormality was no longer observed. These findings suggest that coronary-to-pulmonary artery fistulae potentiated the myocardial ischemia in patient with coronary stenosis leading to unstable angina and prolonged the presence of coronary perfusion abnormality on stress thallium scans probably through a coronary steal phenomenon.

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