To clarify the prognostic significance of signal averaged electrocardiogram (SAE), 100 patients with old myocardial infarction (OMI) and 54 patients with dilated cardiomyopathy (DCM) were studied. Late potentials (LPs) were detected in 31 patients with OMI and in 21 patients with DCM. During a mean follow up of 18 months (3 to 60) in OMI and 28 months (3 to 71) in DCM, 29 patients died. Fifteen patients died suddenly (8 in OMI, 7 in DCM). In OMI, the sensitivity (Se), specificity (Sp), predictive accuracy (PA) of LPs for sudden death were 75%, 72%, and 73%, respectively. The presence of either LPs or prolonged filtered QRS (f-QRS) predicted sudden death with a high Se, and the presence of both LPs and prolonged f-QRS predicted with high Sp and PA. In DCM, Se, Sp, and PA of LPs were lower than those in OMI (Se; 71%, Sp; 66%, PA; 67%). A life table analysis showed that the probability of remaining free from sudden death was significantly lower in patients with LPs than those without them in OMI, but no significant difference was observed between those with and without LPs in DCM. Patients with either LPs or prolonged f-QRS, however, had a significantly higher probability of sudden death in both diseases and no patient with normal SAE died suddenly. SAE was also useful in separating high risk patients in either normal or low cardiac index group in both diseases. Ventricular tachycardia (VT) and % fractional shortening in OMI and only VT in DCM were also useful predictors among other parameters. In conclusion, SAE provides useful information in a noninvasive method to identify patients at risk of sudden death, and patients with normal SAE have a low risk of sudden death in OMI and DCM.

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Comparative long-term performance characteristics of mechanical valves and bioprosthetic valves were analyzed retrospectively among patients who had undergore isolated aortic valve replacement between 1968 and 1987. One hundred sixty-seven patients received either mechanical (n=82) or bioprosthetic (n = 85) valves. The cumulative follow-up was 926 patient-years (mean 6.1 ± 4.7 years, ranging from 0.5 to 20.2 years 100% complete follow-, up). Actuarial survival rate, including operative death, at 10 years was 74 ± 7% for mechanical and 77 ± 7% for bioprosthetic valve recipients. The rates of freedom from thromboembolism, structural valve failure, prosthetic valve endocarditis, and valve re-replacement at 10 years were 77 ± 7%, 100%, 96 ± 2% and 95 ± 3% for mechanical, and 94 ± 4%, 83 ± 8% (p<0.05), 88 ± 5% and 75 ± 8% (p<0.05) for bioprosthetic valve recipients, respectively. Thromboembolism occurred more frequently in the mechanical valve recipients (p<0.01), and structural valve failure in the bioprostheses recipients (p<0.05). There was no mortality at the time of valve re-replacement. Most of the bioprosthesis recipients received no anticoagulation therapy beyond 3 months postoperatively. Cardiac medication in the late postoperative period was not required in 31.3% of bioprosthetic, and 3.2% of mechanical valve recipients (p<0.01). These results show that bioprosthesis in the aortic position exhibits a superb antithrombogenicity and may enable a drug-free state, though its limited durability requires reoperation.

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We studied the effect of nicardipine on the canine cardiovascular system, especially on total blood volume and vascular compliance. Under light halothane anesthesia, nicardipine decreased total blood volume significantly (from 80.0 ± 8.4 ml/kg in the control state to 75.3 ± 8.0 ml/kg under nicardipine administration, p< 0.01), while it increased central circulating blood volume (from 17.1 ± 5.9 ml/kg to 25.5 ± 8.2 ml/kg, p<0.01), increased cardiac output and central venous pressure, and decreased mean arterial pressure (from 134.3 ± 16.2 mmHg to 93.9 ± 17.1 mmHg, p<0.01) and total peripheral resistance. Vascular compliance derived from fluid infusion experiments showed a significant decrease (from 8.9 ± 3.8 ml/ mmHg/kg to 5.5 ± 8.0 ml/mmHg/kg, p<0.01 ). In addition to the vasodilatory action of nicardipine on arteries, these findings also suggest that 1) nicardipine causes a fluid shift from the vascular to the interstitial fluid space as a result of increased capillary pressure, 2) it increases preload through blood redistribution from the peripheral to the central circulation, and 3) it decreases compliance of the vassels, perhaps due to an indirect splanchnic venoconstriction.

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We investigated the presence of α-adrenoceptor subtypes in systemic capacitance vessels by examining the effects of α₁- and α₂-agonists or antagonists on the mean circulatory pressure (MCP). Dogs were anesthetized with pentobarbital, and after total spinal anesthesia, epinephrine was given intravenously to maintain mean blood pressure at about 80 mmHg. l . With intravenous injection of phenylephrine (α₁-agonist, 10 μg/kg, n = 7), and of BHT 920 (α₂-agonist, 5 μg/kg, n = 7), MCP increased significantly from 9.8 ± 0.4 (mean ± SE) to 10.9 ± 0.3 mmHg (+11.2%, p<0.01), and from 9.3 ± 0.4 to 10.3 ± 0.4 mmHg (+10.8%, p<0.05), respectively. 2. Intravenous injection of prazosin (α₁-antagonist, 150 μg/kg, n = 7) and of yohimbine (α₂-antagonist, 30 μg/kg, n = 7) decreased MCP significantly from 9.9 ± 0.4 to 8.2± 0.5 mmHg (-17.2%, p<0.01), and from 9.8 ± 0.2 to 7.6 ± 0.3 mmHg (-22.4%, p< 0.01 ), respectively. 3. Intravenous injection of phenylephrine (10 μg/kg, n = 7) after pretreatment with prazosin (150 μg/kg) decreased MCP significantly from 9.5 ± 0.3 to 7.8 ± 0.3 mmHg (-17.9%, p<0.01). MCP decreased significantly from 9.9 ± 0.3 to 8.2 ± 0.3 mmHg (-17.2%, p<0.01) after intravenous injection of BHT 920 (5 μg/kg, n = 7) following pretreatment with yohimbine (30 μg/kg). These results suggest that the α₁- and α₂-adrenoceptor subtypes exist in systemic capacitance vessels, and that both play a mediating role in systemic venoconstriction induced by their agonists in areflex dogs.

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Pre- and postoperative echocardiograms of 64 patients with chronic aortic regurgitation who had undergone isolated aortic valvular replacement (AVR) were studied. These patients were divided into 3 groups as follows: (1) Group A patients who had preoperative end-diastolic radius to wall thickness ratio (R/Thd) &les; 3. (2) Group B1 patients who had preoperative R/Thd>3 and end-systolic radius to wall thickness ratio (R/Ths)<2. (3) Group B2 patients who had preoperative R/Thd>3 and R/Ths &ges; 2. Using this classification we assessed the relation between the pattern of hypertrophy and left ventricular (LV) function and the reversibility of LV dysfunction following AVR. Preoperatively, ejection fraction (EF) during handgrip exercise was unchanged in Group A (%ΔEF: -2.8 ± 7.1%) and significantly decreased in Groups B1 (-17.0 ± 5.8%) and B2 (-20.2 ± 4.6%). In the late postoperative period, however, it was, -1.2 ± 3.3%, -2.0 ± 4.6%, and -17.7 ± 8.6% in Groups A, B1, B2, respectively. Preoperatively the slope of end-systolic wall stress/volume (ESWS-ESV relation was 1.96 ± 0.43 in Group A (p<0.01 vs Group B2, NS vs Group B1), 1.54 ± 0.38 in Group B1 (NS vs Group B2) and 1.17 :± 0.47 in Group B2. It was stressed that a good relationship existed between the pattern of hypertrophy and function as well as the reversibility of LV dysfunction following AVR.

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In order to evaluate whether there is pulmonary vascular disease in patients with atrial septal defect (ASD), we used the pulmonary vascular input impedance to estimate the stiffness of the pulmonary vessels with before and after surgical intervention. Ten control subjects and 11 patients with ASD (9 operable and 2 inoperable) were examined. In preoperative patients the decreased total pulmonary resistance (Rin) and pulmonary vascular resistance appeared to open new parallel vascular channels with increased blood flow. Further, there were no significant differences in the pulmonary vascular input impedance spectrum and phase, and characteristic impedance among control subjects, preoperative and postoperative patients. Although distensibility of the pulmonary vascular wall in operable patients was similar to that in control subjects, an excessive elevation in Rin and input impedance modulus was observed in inoperable patients. The results demonstrate that the normal input impedance spectrum and phase in patients with ASD is predictive of a good prognosis after successful surgical correction.

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Endothelium-dependent and independent hypotension, vasodilation and relaxation were examined comparatively, in vivo and in vitro, in spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto rats (WKY). In conscious and unrestrained animals, the dose-dependent hypotensive responses to both acetylcholine and adenosine triphosphate (ATP) were attenuated in SHR, compared to findings in the WKY, while sodium nitroprusside lowered mean arterial pressure (MAP), to a similar degree in SHR and WKY. Acetylcholine, ATP and nitroprusside increased the heart rate of SHR and WKY, in a dose-related manner. Mesenteric and femoral blood flow was altered by acetylcholine, ATP and nitroprusside, in a similar manner in the SHR and WKY anesthetized with urethane. However, an ATP-induced reduction in renal blood flow was greater in the SHR than in the WKY. Acetylcholine and nitroprusside led to a concentration-dependent relaxation in the isolated mesenteric artery, to a similar extent in both strains of rats. The relaxation response to acetylcholine was nearly abolished by mechanical removal of the endothelium, but the nitroprusside-induced relaxation was not altered by this denudation. ATP did not influence contraction of the mesentric artery but did produce endothelium-dependent relaxation of aorta, in a dose-dependent manner. All these events suggest that suppression of the endothelium dependent relaxation of resistant arterioles relates to the maintenance of hypertension, in the SHR.

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We studied whether or not neonatal streptozotocin (STZ) treatment would alter mean arterial pressure (MAP) and blood pressure regulating factors in conscious and unrestrained spontaneously hypertensive rats (SHR). Neonatal STZ administration to SHR resulted in type 2 diabetes mellitus with reduced MAP and heart rate. Plasma glucose was markedly increased in these diabetic animals and was inversely correlated with MAP. In the diabetic SHR, the hypotensive responses to captopril (SQ) or enalapril, administered intravenously, were diminished, regardless of preceding administrations of vasopressin V₁-antagonist (AVPA) or hexamethonium (C₆), when compared to findings in control rats. In contrast, the C₆-induced hypotension was similar in rats with diabetes and control animals. AVPA led to no decrease in MAP in either group. Hypotensive responses to SQ following AVPA and C₆ inversely correlated with the plasma levels of glucose in the diabetic group. The combined blockade of the renin-angiotensin system (RAS), sympathetic nervous system and vasoconstrictive action of vasopressin (AVP) abolished the differences in MAP between the groups. Pressor and bradycardic responses to intravenous noradrenaline, angiotensin II and AVP were practically identical in the diabetic and control SHR. Urinary aldosterone excretion rate was not altered by neonatal STZ treatment. In conclusion, a decrease in MAP in SHR with neonatal STZ treatment may be attributed to the suppressed pressor activity of RAS.

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We performed electrical catheter ablation (ECA) in a patient who had old myocardial infarction and drug-refractory sustained ventricular tachycardia (VT). ECA using 100J to the earliest activation site and the pace-mapping site failed to prevent the VT. ECA using the same energy to the site at which mid-diastolic potential was recorded during tachycardia could successfully ablate the VT. Therefore the site of energy delivery was important in VT with old myocardial infarction.

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It is well known that the strength of postextrasystolic potentiation (PESP) is dependent on the prematurity of the ectopic beat, though the fundamental mechanism of the potentiation is still obscure. In this study, the effect of a resting interval on the strength of PESP was investigated in isolated papillary muscles of guinea pigs in the presence or absence of caffeine, which inhibits the functions of sarcoplasmic reticulum (SR). PESP of a fixed coupling interval increased and then decreased as the resting interval was prolonged. The maximum of PESP was obtained at a resting interval of 3 to 4 sec. The dependency of PESP on a coupling interval was decreased considerably by 5 × 10^-4M caffeine and removed completely by 10^-2M caffeine. Although 5 × 10^-4M caffeine decreased the degree of contraction of postextrasystole, the maximum contraction of postextrasystole was still obtained at a resting interval of 3 to 4 sec. After the application of 10²M caffeine, the postextrasystolic contraction gradually declined as the resting interval was prolonged. We conclude that SR Ca release contributes largely to a mechanism of PESP and increases in contribution as the coupling interval of an extrastimulation shortens, and that the optimal resting interval is determined by a balance between the activity of SR function and the activity of the sarcolemmal Ca extrusion mechanism.

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A case of sustained ventricular tachycardia (VT) with two possible exits from one re-entrant circuit is described in this paper. The patient was a 27-year-oId female who had undergone corrective surgery for tetralogy of Fallot at the age of 8, and developed VT of distinctly different QRS configurations. The exit of one VT was at the right ventricular (RV) outflow tract and the other at the RV apex as determined by endocardial and pace-mapping. Continuous and split activities were observed at the RV outflow tract during both types of VT. One VT was entrained by rapid pacings, and the causal mechanism was thought to be re-entry and common re-entrant circuit was established for two QRS configurations of VTs. A discrepancy was observed between the site of the earliest activation and the site of the pace-mapping which resulted in QRS configuration of VT of the RV apex origin. The findings in this paper should be considered when contemplating aggressive therapy such as electrical ablation.

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