Rapid growth of the cardiac left ventricle is a hallmark of the neonatal period. During the first 2 weeks of life in the piglet, weight of the left ventricle increases 4 fold. The increase in weight is accompanied by approximately a 4 fold increase in myocyte volume indicating hypertrophic growth. Total RNA also increases approximately 4 fold indicating that the mechanism of growth involves greater ribosome content and greater capacity for protein synthesis. The rapid rate of ribosome formation and protein synthesis cannot be further accelerated in isolated perfused hearts by insulin, agents that increase 3',5'-cyclic monophosphate, α₁-adrenergic agonists or angiotensin II. In an attempt to slow cardiac growth and make it responsive to growthpromoting agonists, piglets are treated with an angiotensin converting enzyme inhibitor, enalapril maleate. Enalapril decreases left ventricular growth by 19% and total RNA content by 36%. When enalapril-treated hearts are perfused in vitro for 1 h, α₁-adrenergic agents restore rates of ribosome formation to control values but angiotensin II has no effect. In left ventricular myocytes that are cultured for 3 days, an α₁-adrenergic agonist and endothelin increases the rate of protein synthesis by 20 to 75% but angiotensin II has only a marginal effect (8%). These findings indicate that inhibition of growth by enalapril most likely is due to decreased ventricular pressure development that is secondary to peripheral vasodilation and a fall in mean arterial pressure. (Jpn Circ J 1997; 61: 645 - 649)

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A Microvolt-1evel T-wave alternans (alternating morphology from beat to beat) during atrial pacing and exercise may predict ventricular tachycardia (VT) and fibrillation (VF) in ischemic heart disease. We tested whether such alternans during exercise could identify high-risk patients with hypertrophic cardiomyopathy (HCM). We studied 14 HCM patients and 9 normal control subjects for T-wave alternans using the CH2000 system with 7 multisegment electrodes in a Frank orthogonal (XYZ) configuration. Bicycle ergometer exercise was used to increase the heart rate (HR) to 95-110 beats/min. Seven patients were at high risk for ventricular arrhythmias (1 with sustained VT, 3 with abnormal paced ventricular electrograms as seen in VF survivors, and 3 with nonsustained VT and/or an adverse family history), and the other 7 were at low risk. T-wave alternans was present if alternans >1.9 μV was consistently present with the HR in excess of a patient-specific HR threshold. Alternans was found in 5 of 7 high-risk patients (71%) vs none of 7 low-risk patients or 9 control subjects (p<0.025 and p<0.01, respectively). Notably, all 4 patients with sustained VT or abnormal ventricular electrograms showed alternans. Thus, high-risk patients with HCM often show T-wave alternans. Microvolt-1evel alternans during exercise may be a useful marker for ventricular arrhythmic risk in patients with HCM. (Jpn Circ J 1997; 61: 650 - 656)

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The level of tumor necrosis factor alpha (TNF-α) is increased in patients with congestive heart failure and may play an important role in the development and progression of heart failure. Two types of TNF receptor (TNF-RI and TNF-RII) are expressed in virtually every cell and have different biologic roles. Soluble forms of the two receptors (sTNF-RI and sTNF-RII) have been identified as extracellular domain fragments. Serum levels of TNF-α, sTNF-RI and -RII were measured in 66 patients with heart failure and 27 control subjects using an enzyme-linked immunosorbent assay (ELISA). Hemodynamic variables, norepinephrine, atrial natriuretic peptide (ANP) , and brain natriuretic peptide (BNP) were evaluated. TNF-α was significantly higher in patients with heart failure than in control subjects (9.4±1.4 vs 4.8±0.8 pg/ml; p<0.05). sTNF-RI and -RII were significantly increased in relation to the severity of heart failure (control subjects, 0.66±0.04 and 1.97±0.15 ng/ml; NYHA class II, 1.10±0.08 and 2.28±0.12 ng/ml; NYHA class III, 1.63±0.22 and 3.00±0.24 ng/ml; NYHA class IV, 2.78±0.46 and 4.52±0.62 ng/ml, respectively). In 9 patients whose clinical symptoms improved after treatment, the levels of sTNF-RI and -RII decreased by 17.3 ±5.7% (p<0.05) and 22.1±6.9% (p<0.05), respectively. There were significant positive correlations between sTNF-RI and -RII and mean pulmonary pressure (r=0.69 and r=0.61; p<0.001) and mean capillary wedge pressure (r=0.65 and r=0.54; p<0.001 and p<0.01, respectively), but not with left ventricular end-diastolic volume or ejection fraction (NS). sTNF-RI and -RII were also significantly positively correlated with plasma levels of norepinephrine (r=0.75 and r=0.50; p<0.001 and p<0.05), ANP (r=0.72 and r=0.70; p<0.001), and BNP (r=0.60 and r=0.60; p<0.001). In conclusion, soluble TNF receptors are increased in proportion to the severity of congestive heart failure and may reflect the current status of congestive heart failure rather than the level of left ventricular dysfunction. (Jpn Circ J 1997; 61: 657 - 664)

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We evaluated quantitatively the correlations between resting wall motion and regional myocardial blood now (RMBF; at rest and during exercise) in infarct-related myocardium. The study was performed in 28 subjects: 21 patients who had previously suffered myocardial infarction of the anteroseptal wall, and 7 normal individuals. Positron emission tomography (PET) with [¹³N]ammonia was performed at rest and during low-grade exercise (bicycle ergometer fixed at 25 W for 6.5 min), and RMBF was measured quantitatively from the radioactivity in myocardial tissue and arterial blood. Resting regional wall motion was calculated using the centerline method on left ventriculographic findings. Resting regional wall motion was correlated with RMBF both at rest and during exercise in the infarct areas (anterior walls: y= -2.74+4.25×10 ^-2x, r=0.43, at rest; and y=-2.48+3.04×10 ^-2x, r=0.48, during exercise, p<0.05; septal walls: y=-3.61+5.64×10^-2x, r=0.62, at rest; and y=-3.46+4.31×10^-2x, r=0.62, during exercise, p<0.01). In each infarctielated wall, the coefficient (the slope) during exercise was smaller than that at rest (3.04 vs 4.25 and 4.31 vs 5.64 in each), and the infarct areas with preserved wall motion showed higher RMBF during exercise than those with reduced wall motion. Our results may show that wall motion depends on viable but ischemic myocardium in infarct-related walls. (Jpn Circ J 1997; 61: 665 - 672)

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The clinical outcome and the incidence of ischemic strokes in patients with hypertrophic cardiomyopathy (HCM) with and without atrial fibrillation (AF) were examined. Eighty-three patients with HCM, complicated by AF in 19 patients, and 131 patients with AF but without HCM were studied retrospectively. Primary endpoints (ischemic strokes or cardiac death, whichever occurred first) and ischemic strokes were examined by Kaplan-Meier curves. In the patients with HCM, the primary endpoints occurred more frequently in those with AF than in those without AF (event rate at 5 years 23.0% vs 12.3%, p<0.01). Similarly, the frequency of ischemic strokes in HCM was also much higher with AF than without AF (23.0% vs 5.9% at 5 years, p<0.01). According to multivariate Cox analysis, the strong independent risk factor for ischemic strokes in HCM was AF (p<0.01), whereas in patients with AF they were HCM (p<0.01) and age (p <0.01). These results suggest that incidence of ischemic strokes in HCM is markedly increased if complicated by AF as compared with that in patients with AF alone. (Jpn Circ J 1997; 61: 673 - 681)

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The CryoLife-O'Brien stentless valve is a composite trileaflet porcine aortic valve. It is assembled from 3 non-coronary leaflets and has no foreign material support. It is therefore truly stentless. From December 1992 to January 1996, 118 patients with aortic valve replacement had a CryoLife-O'Brien stentless valve inserted at the Prince Charles Hospital, Brisbane. The mean age was 73 years (range 59-89) and 54% were men. Most patients had aortic stenosis secondary to a calcific degenerative valve. Follow-up is 100% with hematological and echocardiographic studies before discharge, at 6 months, and at 12-18 months. Five deaths (2 early and 3 Iate) have occurred and morbidity includes 3 strokes, 1 peripheral embolism, 3 perivalvular leaks, and 1 patient with late endocarditis. Valve performance has been good, with low transvalvular gradients and only a trace or no regurgitation in over 95% of patients after 18 months. No structural deterioration or hemolysis has occurred. Echocardiographic surveillance confirms a very effective central orifice. Short-term results show that the overall performance of the CryoLife-O'Brien stentless valve has been very satisfactory, with low mortality and morbidity in this elderly group of patients. The benefits include the absence of prosthetic material, wide leaflet coaptation, and a quick and easy insertion. Long-term anticoagulation is not necessary. It is particularly suitable for elderly patients with a symmetrical aortic root. (Jpn Circ J 1997; 61: 682 - 686)

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This study was undertaken to examine whether a sulthydryl-containing angiotensin-converting enzyme (ACE) inhibitor, captopril, improves postischemic cardiac function and myocardial metabolism in the perfused working rat heart, and to elucidate the mechanism by which captopril protects the myocardium from postischemic damage. Isolated rat hearts were perfused by the working heart technique for 15 min. Ischemia was then induced for 30 min by lowering the afterload pressure and coronary flow to zero. After ischemia, hearts were reperfused for 30 min by returning afterload pressure to 60 mmHg. Captopril, a non-sulfhydryl-containing ACE inhibitor, enalapril, or a type 1 angiotensin II receptor antagonist, DuP753, was added to the perfusate 5 min before ischemia, and the treatment was continued during the first 10-min period of reperfusion. In all groups there was no significant difference in pressure-rate product, coronary flow, tissue levels of ATP, total adenine nucleotides (TANs), energy charge potential (ECP), or creatine phosphate (CrP) before and during ischemia. During reperfusion following ischemia, captopril significantly improved the recovery of pressure-rate product, coronary flow, and tissue levels of ATP, TAN, ECP, and CrP, but neither enalapril nor DuP 753 had an effect. In conclusion, captopril improved postischemic cardiac function and myocardial metabolism in the perfused rat heart and its effect was independent of the blunting of angiotensin II formation. (Jpn Circ J 1997; 61: 687 - 694)

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The feasibility of transcatheter laser ablation of the canine left ventricle (LV) was tested using a newly developed cardioscope. In 17 anesthetized dogs, a combined laser-endoscope catheter, consisting of an endoscope encased in a 7-French flexible catheter with an inflatable and transparent balloon at the distal end, was introduced into the LV via the carotid artery. A 1064-nm neodymium-yttrium-aluminum-garnet (Nd:YAG) laser was delivered by laser optic fiber, which was introduced through the transport channel and positioned inside the saline-filled balloon. In 16 of 17 dogs, the endocardial surface of the LV was clearly observed. Laser energy totaling 500-5,000 J was applied sequentially in 13 dogs and laser irradiation was completed in all but 2 of the dogs. The excised hearts revealed well-demarcated oval-shaped lesions 2.5-9.5 mm deep in 7 of 11 dogs. Histologic sections revealed coagulation necrosis surrounded by a rim of contraction band necrosis. Thus, transballoon laser photocoagulation of the beating LV is feasible. The newly combined laser-endoscope catheter, which is still in its preliminary stages and needs to be improved to increase the success rate of photocoagulation, appears to be a promising alternative modality for catheter ablative therapy for ventricular tachycardia. (Jpn Circ J 1997; 61: 695 - 703)

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We developed an organ culture system in order to examine the effect of intraluminal pressure on intimal thickening in injured arteries. After endothelial denudation, an excised rabbit common carotid artery was incubated at 37°C in a glass bottle perfused with Dulbecco's modified Eagle medium containing 10% fetal calf serum at a constant flow rate of 6 ml/h at various static pressure of 60, 95, 130, 165, or 200 cmH₂O. Intimal thickening, which consisted of smooth muscle cells and extracellular matrix, increased in a time- and pressure-dependent manner up to 130 cmH₂O. Excessive pressures (165 and 200 cmH₂O), however, caused necrosis in the media. These results suggest that a rise in intraluminal pressure accelerates intimal thickening in injured arteries. (Jpn Circ J 1997; 61: 704 - 708)

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Ischemic preconditioning is known to be mediated by several humoral factors, such as adenosine, norepinephrine, and bradykinin. We examined intracellular signal transduction of ischemic preconditioning following receptor stimulation. Alterations in the pH of the ischemic bed were monitored to assess the response of control and ischemic-preconditioned myocardium to glibenclamide and pertussis toxin. Pentobarbital-anesthetized open-chest dogs were subjected to 40 min of ligation of the left anterior descending coronary artery. Ischemic preconditioning was elicited by 25-min periods of coronary ligation followed by 5 min of reperfusion before a 40-min period of ligation. Glibenclamide (0.3 mg/kg) was given iv 20 min before the onset of ischemic preconditioning. Pertussis toxin (6-10μg/kg) was given iv 3 days before the experiment. Tissue myocardial pH was measured by a glass micro-pH electrode. Ischemia for 5 min decreased myocardial pH and reperfusion returned it to the preischemic levels. Ischemia for 40 min decreased the myocardial pH from 7.43±0.06 to 6.43±0.08. Ischemic preconditioning significantly attenuated the decrease in myocardial pH (6.57±0.06) induced by 40 min of ischemia. Pretreatment with either glibenclamide or pertussis toxin completely abolished the effect of ischemic preconditioning on ischemic myocardial acidosis. Ischemic preconditioning can attenuate ischemia-induced myocardial acidosis in dogs, and this effect is mediated by activation of adenosine triphosphate-sensitive potassium channels and pertussis toxin-sensitive guanosine triphosphate-binding protein. (Jpn Circ J 1997; 61: 709 - 714)

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A 65-year-old man was admitted with a diagnosis of arteriosclerosis obliterans. He had a 3-month history of intermittent claudication of the right leg. Physical examination revealed absence of pulsation of the right posterior tibial artery. Contrast angiography of lower extremities showed several severe obstructive lesions below the right popliteal artery. As interventional and surgical approaches were not indicated, the patient was treated with exercise with heparin pretreatment (5,000 IU). As a result, walk distance on a floor was increased from 400 m to 2,000 m, and repeat magnetic resonance angiography revealed increased flow to the right lower extremity. Thus, he was successfully treated with exercise and heparin pretreatment without any side-effects. (Jpn Circ J 1997; 61: 715 - 718)

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A 54-year-old woman was admitted to our hospital because of a heart murmur without subjective symptoms. Angiography disclosed an enlarged right coronary artery and flow drainage into the left ventricle, ie, a large right coronary artery-left ventricle fistula. Analysis of pulsed Doppler studies and cineangiograms indicated considerable capacitance of this fistula owing to Windkessel action, which attenuated volume overload on the left ventricle. The features in this case suggest that evaluation of fistula hemodynamics is important in deter-mining the overload on the ventricle through the fistula. (Jpn Circ J 1997; 61: 719 - 723)

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(Jpn Circ J 1997; 61: 724-725)

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