The effect of sodium bicarbonate haemodialysis or haemofiltration on cardiac function was prospectively studied in 8 patients with acute renal failure. All of the patients exhibited consciousness disturbance and seven patients were on mechanical ventilation. All but one of the patients demonstrated moderate hyperlactataemia and seven patients were receiving vasoactive amine support. Arterial and mixed venous gas analysis and haemodynamic measurements were performed before and after haemodialysis/-filtration treatment. The buffer was changed in a randomised order between bicarbonate and acetate and 11 crossover studies were completed. After treatment with bicarbonate, the cardiac index and stroke index decreased significantly (4.0±0.3 to 3.4±0.4 L/min/m², p<0.05 and 39.6±2.5 to 32.9±1.8 L/m², p<0.05), whereas no significant changes were observed in cardiac index or stroke index after treatment with acetate. Therefore, the post-dialytic percent changes of cardiac index, stroke index and left ventricular stroke work index were significantly decreased after bicarbonate sessions, as compared to after acetate sessions. Haemo-dialysis/ -filtration using sodium bicarbonate can depress cardiac function in critically ill patients on mechanical ventilation with disturbed consciousness, and in those who are receiving vasoactive amine support due to uncompromised haemodynamics associated with hyperlactataemia.

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Long-term changes in regional wall motion (RWM) following acute myocardial infarction (AMI) in 42 patients with uncomplicated single-vessel disease were examined retrospectively by repeat cardiac catheterizations. The first and second cardiac catheterizations were performed at an average of 28 days and 6.6 years after the onset of AMI, respectively. All 42 patients underwent first and second cardiac catheterizations without undergoing coronary artery bypass surgery or coronary angioplasty. Regional left ventricular functions were analyzed by the centerline method using a right anterior oblique left ventriculogram. The wall motion abnormality score (WMAS) was defined as [#chord below -2SD] × [mean SD chord below -2SD]. The improvement in the WMAS was more prominent in cases with an occluded infarct-related artery. Thus, we concluded that 1) RWM improves significantly with medical treatment in long-term follow-up in cases of uncomplicated AMI with single-vessel disease, and 2) the improvement of RWM is completed within the first few weeks after AMI in cases with a patent infarct-related artery.

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To determine the role of the accessory pathway in the pathogenesis of atrial fibrillation, we compared electrophysiological findings in 17 patients (44.7±10.2 years) with a history of atrial fibrillation before and after surgical ablation of the accessory pathway. The PA interval was shortened, and the atrial refractory periods and the potential minimal wavelength of an atrial impulse (FRP_A/PA) were significantly increased, after surgery. Fragmented atrial activity (an increase of 150% or more in the duration of the high right atrial electrogram) was observed in 80% of the patients before surgery and in 25% after surgery. Its zone was significantly decreased after surgery. Repetitive atrial firing was defined as the occurrence of 3 or more successive atrial electrograms induced by a premature stimulation. This was observed in 60% of the patients before surgery, but in none after surgery. Atrial fibrillation was induced in 16 patients during the preoperative study, but in only 1 patient postoperatively. In conclusion, these results suggest that accessory pathways affect atrial vulnerability and play an important role in the onset of atrial fibrillation in WPW syndrome.

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Numerous attempts have been made to prevent late restenosis after successful percutaneous transluminal coronary angioplasty (PTCA), but there is still no effective treatment. This report describes the effect of an oral lipid-lowering agent, pravastatin, on restenosis after successful PTCA. Sixty-six patients who underwent successful elective PTCA were assigned to a pravastatin-treated group (Group 1, n=29) or an untreated group (Group 2, n=37) in a prospective and randomized fashion. Pravastatin (5 mg or 10 mg twice a day) was given to Group 1 patients from day 3 after the procedure. Selective coronary angiography was repeated 3 to 5 months later, or sooner if the patient developed angina pectoris. The serum cholesterol level was decreased significantly in Group 1 (from 215.7±44.3 mg/dl to 181.2±30.3 mg/dl, p<0.001), but not in Group 2 (from 191.9±30.8 mg/dl to 191.8±33.3 mg/dl, p=ns), at the time of repeat coronary angiography. However, there were no differences between the groups with regard to the recurrence of angina, the need for repeat PTCA, or restenosis, as assessed by quantitative analysis of coronary cineangiograms. These results suggest that oral pravastatin therapy does not effectively prevent late restenosis after successful PTCA by this mode of administration.

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To assess the clinical value of simultaneous dual myocardial imaging with iodine-123-β-methyl-iodophenyl-pentadecanoic acid (¹²³I-BMIPP) and thallium-201 (²⁰¹Tl), myocardial imaging was performed at rest and during exercise in seven patients with coronary heart disease. When ¹²³I-BMIPP and ²⁰¹Tl images were compared, the initial exercise and resting images agreed 87% and 64%, respectively. In the initial resting images, the regional uptake of ¹²³I-BMIPP was frequently less than that of ²⁰¹Tl. The incidence of exercise-induced reversible defects by ²⁰¹Tl in the Tl>BMIPP regions was significantly higher than that in the Tl=BMIPP regions (57% vs 4%, p<0.01) and the incidence of coronary narrowing of more than 90% in the Tl>BMIPP regions was also significantly higher than that in the Tl=BMIPP regions (91% vs 38%, p<0.01). In addition, this disparity (Tl>BMIPP) was found more frequently in regions with abnormal wall motion than in regions with normal wall motion (hypokinetic regions; 68%, severe hypokinetic or akinetic regions; 50%, vs normokinetic regions; 4%, p<0.01). In contrast, the uptake of ¹²³I-BMIPP correlated closely with that of ²⁰¹Tl in normal myocardium and the uptake of both ¹²³I-BMIPP and ²⁰¹Tl was severely reduced in myocardium with severe ischemia during exercise and prior infarction. These results indicate that dual myocardial imaging with ¹²³I-BMIPP and ²⁰¹Tl may provide a unique means of identifying patients with metabolically disturbed myocardium, such as hibernating and stunned myocardium.

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Left ventricular (LV) performance of the pharmacologically regressed heart in hypertension is still unclear. We compared LV function of the heart regressed by nifedipine with that of the hypertrophied heart in spontaneously hypertensive rats (SHR). Nifedipine (30 mg/kg/day in food) was given to 15-week-old male SHR for 20 weeks (n=12). Age- and sex-matched SHR served as controls (n=12). LV catheterization was performed using a micromanometer and cardiac output was determined by the thermodilution method. Hemodynamic studies were performed after washout of nifedipine (24 h), when blood pressure had returned to the untreated level. Peak pumping ability was assessed during acute volume loading with saline, Nifedipine significantly decreased blood pressure in conscious animals (222±11 to 201±12 mmHg, p<0.01) and reduced LV weight (1.20±0.07 to 1.07±0.05g, p<0.01). After washout of nifedipine, LV systolic and end-diastolic pressures, dp/dt_max and cardiac output determined under pentobarbital anesthesia were similar in the treated and untreated groups. Peak pumping ability during acute preload elevation was also similar in the 2 groups. Plasma norepinephrine was unaltered, and plasma renin activity was significantly lower in the treated rats (p<0.05). These results indicate that nifedipine regressed LVH with a minimal reduction of blood pressure and without evidence of neurohumoral activation or volume retention. In conclusion, LV function of the heart regressed by nifedipine was preserved after a spontaneous rise in blood pressure and during acute preload elevation.

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To investigate the pathologic changes of the myocardium and the adverse effects of radiogrequency (RF) catheter ablation, we observed canine hearts that had been ablated by RF energy. Catheter ablation was administered to three sites of the hearts of 46 dogs: endomyocardium, coronary sinus, and atrioventricular junction. The dogs were sacrificed 0-12 weeks after ablation and the lesions were stained with hematoxylin-eosin and Azan stain. Each ablated lesion was well demarcated from the adjacent normal tissue. The margin between the ablated lesion and normal tissue became clearer with time. The lesions were hemispherical and measured about 2 to 10 mm in diameter and 1 to 6 mm in depth. Histologic examination in the acute phase demonstrated the presence of coagulation necrosis of the myocardium, interstitial hemorrhage and edema, followed by infiltration of inflammatory cells. Granulation tissue replaced the normal myocardium. In the chronic phase, the lesions became fibrotic and fatty. A mural thrombus was found in 30% of the cases of endomyocardial ablation and 50% of the right ventricular lesions were transmural. Ablated lesions in the coronary sinus extended to the left atrium and left ventricle. Obstruction of the coronary sinus was observed in 8% of the ablated dogs. Most of the lesions with complete atrioventricular block were ablated at the His penetrating region of the conduction system. Thus, since the ablated lesions were clearly delineated, catheter ablation using RF energy appears to eliminate only the target area.

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Effects of α-human atrial natriuretic polypeptide (α-hANP) on renal function were studied in anesthetized dogs and isolated perfused rat kidneys. Two doses of α-hANP were used to determine whether renal hemodynamics or tubular reabsorption is tha major factor in the diuretic action of α hANP. The excretion rates of sodium (Na) and inorganic phosphate (PO₄) were evaluated to determine the site of diuretic action in the renal tubule. In dogs that received the smaller dose of α-hANP (5 ng.kg^-1.min^-1) infused into the renal arteries without changes in systemic or renal hemodynamics, urine volume (UV) and urinary Na excretion (UNaV) increased significantly. Fractional excretion of Na (FENa) was increased, while fractional excretion of PO₄ (FEpo4) was unchanged, following the infusion of α-hANP. The calculated fractional Na reabsorption in the distal tubule (DTRNa) during the infusion of α-hANP was significantly suppressed. In dogs that received the a larger dose of α-hANP (50 ng.kg^-1.min^-1), the glomerular filtration rate (GFR), UV, and FENa were increased and DTRNa was decreased. In isolated rat kidneys perfused at a constant pressure, a lower concentration of α-hANP (0.5 ng.ml^-1) in the perfusate caused diuresis and increased Na and PO₄ excretion without any renal hemodynamic alterations. A higher concentration of α-hANP (5 ng.ml^-1) increased GFR, Na and PO₄ excretion. Since PO₄ reabsorption is believed to occur primarily in the renal proximal tubule, these findings suggest that the diuretic action of α-hANP in smaller doses is induced by direct action on renal distal nephron. However, the site of action of α-hANP in larger doses was not determined in the renal tubule because GFR and FEPO₄ increased and DTRNa decreased following infusion of α-hANP.

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A 62-year-old patient was admitted to our hospital for treatment of early gastric cancer. After total gastrectomy, he suffered from anteroseptal myocardial infarction. Systolic anterior motion of the mitral valve which was not observed before surgery was observed during the acute phase of myocardial infarction and completely disappeared 3 weeks after the onset of myocardial infarction. Systolic anterior motion of the mitral valve in this patient may have been caused by changes in left ventricular wall motion during the acute phase of myocardial infarction .

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We present a 74-year-old female who showed a large left-to-right shunt through a small atrial septal defect presumably due to diastolic dysfunction of the left ventricle caused by the progression of aortic stenosis. Accordingly, elderly patients with even small atrial septal defect should be followed carefully, since diastolic dysfunction of the acquired left ventricular disorder could increase the left-to-right shunt.

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