Cardiogenic pulmonary edema is a frequent cause of reparatory failure. We investigated the effects of nasal continuous positive airway pressure (CPAP) in patients with severe pulmonary edema associated with acute myocardial infarction. Twenty-nine consecutive patients were divided into 3 groups: firstly, 7 intubated patients who received mechanical ventilation at study entry comprised the intubation group. The rest of the patients were randomly assigned to either of the following 2 groups: 11 patients who received oxygen plus CPAP delivered by a nasal mask (CPAP group), and 11 patients who received oxygen only via face mask (oxygen group). All patients in the intubation group had cardiogenic shock. Two patients (18%) in the CPAP group and 8 patients (73%) in the oxygen group required mechanical ventilation with endotracheal intubation (p=0.03). The hospital mortality rate in the CPAP group (9%) was significantly lower than the oxygen group (64%, p=0.02). The pulmonary artery wedge pressure and heart rate were significantly lower in the CPAP group than in the oxygen group 24 h after study entry (p<0.05 and p<0.01). The mean pulmonary artery pressure 48 h after study entry was 18±5 mmHg in the CPAP group and 25±8 mmHg in the oxygen group (p<0.05). The PaO₂/FiO₂ ratio increased in the intubation group (168±69 to 240 ±57, p<0.05) and the CPAP group (137±17 to 253±67, p<0.01) 24 h after study entry. Arterial plasma endothelin-1 concentrations decreased significantly earlier in the CPAP group than in the oxygen group (p<0.05). In patients without cardiogenic shock, nasal CPAP lead to an early improvement in oxygenation and hemodynamics, and decreased the mortality rate. Early and active respiratory management is recommended in patients with pulmonary edema associated with acute myocardial infarction. (Jpn Circ J 1998; 62: 553 - 558)

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This study was designed to clarify the efficacy of coronary artery bypass grafting (CABG) on left ventricular (LV) function in 16 patients with a dilated LV due to myocardial infarction (LV end-systolic volume index: LVESVI >60 ml/m²). All had attained complete revascularization. To estimate the LV wall motion quantitatively using echocardiography, a wall motion score (WMS) was used (LV was divided into17 segments with a four-point scale: akinesis=3, severe hypokinesis=2, hypokinesis=1, normal=0 and then summed). Exercise stress tests were performed after surgery, revealing that anginal symptoms had vanished in all the patients. In 5 patients with a preoperative end-systolic volume index (ESVI) >100 ml/m², the ejection fraction (EF) did not change, and both were under 30% (before to after: 26±4 to 26±4%). Neither the ESVI (148±50 to 133±39 ml/m²) nor the end-diastolic volume index (end-diastolic volume index (EDVI): 198±62 to 180±37 ml/m²) changed; the WMS did not change (33±2 to 33±3). During exercise, in spite of the increase in heart rate (HR) (at rest, 81±20; HR during exercise, 111±21 beats/min, p<0.005) and LV end-diastolic pressure (EDP) (22±9; 35±13 mmHg, p<0.02), both cardiac index (CI) (2.4±0.3; 2.6±0.4 L/min·m²) and minute work (MW: 4.0±1.1; 4.1±0.4 kg·M/min) did not increase. In 11 patients with a preoperative ESVI <100 ml/m², EF was extremely increased in 5 patients (more than 10%, 35±4 to 60 ±6%, p<0.005= improved subgroup) in whom the EDVI (130±16 to 120±13 ml/m²) did not change whereas the ESVI (82±14 to 48±7 ml/m²) was reduced. However, in the 6 remaining patients (ie nonimproved subgroup), neither ESVI (78±8 to 74 ±12 ml/m²), EDVI (115±10 to 115±20 ml/m²) nor EF (31±7 to 35±3%) changed. During exercise, HR (at rest, 88±13; during exercise, 108±11 beats/min, p<0.005), LVEDP (20±6; 29±7 mmHg, p<0.01), CI (2.5±0.6; 3.3±0.5 L/min·m², p<0.05), MW (4.6±1.0; 6.5±1.5 kg·M/min, p<0.05) increased. The WMS in the nonimproved subgroup did not change (29±6 to 27±2), but in the improved subgroup it reduced after surgery (27±3 to 19±4, p<0.01). These data suggested that CABG in patients with a dilated LV was effective against anginal symptoms, but was restricted to left ventricular function. It may be possible to estimate postoperative LV function, including exercise tolerance, from the preoperative LVESVI. (Jpn Circ J 1998; 62: 565 - 570)

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Recent studies have suggested that the attenuation of the local electrogram amplitude recorded from the ablation electrode during radiofrequency (RF) application predicts lesion growth. This study examined the time course of local electrogram amplitude during ongoing RF delivery in patients with common atrial flutter (AFl). In 71 patients with AFl, RF energy was applied to the anatomical isthmus. Termination of AFl was noted during 68 of 625 applications of RF energy. The changes in local atrial electrogram amplitude observed at all successful sites were analyzed. With increasing duration of the RF delivery, the electrogram amplitude decreased exponentially to reach a steady state within a mean duration of 17±3 sec, which was significantly longer than that of the steady-state temperature. The average decrease in the amplitude was 67±13%. In 16 patients in whom an increase in the power of RF energy had resulted in AFl termination, there was a dose-response relationship between the power and the amplitude decrease. The decrease in local electrogram amplitude appears to be a reliable marker for the efficacy of tissue heating and may be useful as an endpoint for individual applications. Local electrogram monitoring may offer an optimal energy strategy in AFl ablation. (Jpn Circ J 1998; 62: 559 - 564)

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Intermittent transdermal therapy of nitroglycerin (NTG) has been recommended for the prevention of nitrate tolerance, but a rebound phenomenon has been reported to occur following removal of the NTG tape. The present study investigated the effects of intermittent NTG therapy on vasodilatory response and the intracellular production of cyclic GMP (cGMP). The study group comprised 12 healthy adults and measurements were taken of the platelet cGMP level, the venous volume (VV) (by forearm plethysmography) and the plasma levels of neurohormonal factors before and 5 min after administration of 0.3 mg of sublingual nitroglycerin (NTG) during the following 4 phases: (i) the control phase (8.00 h); (ii) the continuous phase (8.00 h; 7 days after continuous application of a 10 mg/24 h NTG tape); (iii) the intermittent application phase (8.00 h; 7 days after intermittent application of NTG tape, applied at 21.00 h and removed at 9.00 h); and (iv) the intermittent removal phase (13.00 h; 4 h after removal of the NTG tape in the intermittent phase). The percentage increase in cGMP (%cGMP) and venous volume (%VV) were significantly lower in the continuous phase than the control phase, but there was no difference between the control and the intermittent application phases. However, in the intermittent removal phase, the cGMP level before sublingual NTG, the %cGMP and the %VV were unchanged, but the VV before sublingual NTG was significantly lower than in the control phase. Plasma renin activity and the plasma level of angiotensin II were significantly increased in the continuous phase, the intermittent application phase, and the intermittent removal phase. In conclusion, intermittent transdermal NTG therapy prevented nitrate tolerance in the production of cGMP and vasodilation, but induced a rebound phenomenon after removal of the NTG tape. The rebound phenomenon following the tape removal may be related to some other mechanism, such as activation of neurohormonal factors. (Jpn Circ J 1998; 62: 571 - 575)

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We previously reported that cubital venous pressure (Pv) tended to increase initially, but this was followed by a drop in a dose-dependent response after intravenous lidocaine administration in subjects with various diseases. In this study we examined whether Pv responses after small-dose intravenous lidocaine administrations are related to the stimulating effect of lidocaine on vascular smooth muscle (VSM). In 5 subjects free of cardiovascular disease, Pv increased slightly with decreased pulsations after a 10 mg dose (p<0.01) with no change in central venous pressure. In the cinephlebographic test performed on 2 healthy volunteers, Pv increased during recovery from proximal venoconstriction caused by an injection of contrast medium mixed with 10 mg lidocaine. In 9 subjects with cardiovascular disease, ΔPv spread in the same directions (+ or -) after 5 and 10 mg drug administrations. In 6 of those tested with both drug doses, ΔPv had positive means and no significant difference was observed. Thus, Pv responses after small-dose lidocaine administrations are consistent with neither the stimulating effect of lidocaine nor with a dose-dependent response. They could be attributed to the spasmolytic effect of lidocaine on the basal tone of VSM, which could be modulated by disease conditions. (Jpn Circ J 1998; 62: 576 - 580)

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This clinical investigation was designed to determine the effect of changes in loading patterns on left ventricular (LV) relaxation when heart rate was maintained constant. Not only were changes noted in total load or time in which load is changed, but also the contour of the ascending aortic systolic pressure wave. Twenty patients were studied. LV and ascending aortic pressure were measured by a multisensor catheter under baseline conditions (C) and after an intravenous injection of 2.5 μg angiotensin (A) and sublingual administration of 0.3 mg nitroglycerin (N). A bipolar pacing catheter was placed in the right atrium to maintain a constant heart rate throughout the protocol. The augmentation index (AI), which characterizes the contour of the ascending aortic systolic pressure wave, was defined as the ratio of the height of the late systolic shoulder/peak to that of the early systolic shoulder/peak in the pulse. The rate of isovolumic LV pressure decline was calculated as a time constant (Tau). Ascending aortic systolic pressures (mmHg) were 127±29 (C), 158±20 (A) and 109 ±15 (N). AI were 1.61±1.14 (C), 2.08±1.11 (A) and 1.27±1.14 (N). Tau values (msec) were 49±4 (C), 54±4 (A) and 45±5 (N). Tau was prolonged proportionally with increasing AI (p<0.001, r=0.64). It was concluded that late systolic pressure augmentation in the ascending aorta is one important factor that influences the rate of isovolumic left ventricular pressure decline in humans. (Jpn Circ J 1998; 62: 581 - 585)

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This study was undertaken to evaluate the diagnostic value of a new device, the `EAGLE' computer-assisted multiple-lead long-term electrocardiography (ECG) monitoring and analyzing system, in patients with suspected unstable angina, and to compare the results with the Holter monitor. A total of 101 patients with a history of suspected unstable angina underwent a simultaneous 24-h examination with the EAGLE and 2-channel Holter monitors. The diagnosis of unstable angina was established in 70 patients: 41 had significant organic stenosis, and 29 had coronary spasm. Ischemic ST deviations were detected 229 times in 44 patients (62.9%) with the EAGLE system and 101 times in 20 patients (28.6%) with the Holter monitor. The sensitivity of myocardial ischemia in unstable angina with the EAGLE system was significantly higher than that with Holter monitor (62.9 vs 28.6%, p<0.05). The difference of sensitivity was due mainly to the low detection rate of the Holter monitor for asymptomatic myocardial ischemia (EAGLE vs Holter ; 187 times vs 72 times) and myocardial ischemia in the infero-posterior area in patients with organic stenosis (30 times vs none). It is concluded that the EAGLE system is a sensitive tool for the diagnosis of unstable angina in patients without significant ECG changes, and an excellent tool for evaluating silent myocardial ischemia or myocardial ischemia of the infero-posterior area. (Jpn Circ J 1998; 62: 586 - 591)

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An increase of ^99mTc-sestamibi uptake in the myocardium during exercise was defined as a response rate, and the feasibility of a response rate for detecting coronary artery disease (CAD) was tested. Eighty-seven patients with suspected CAD had myocardial perfusion imaging with ^99mTc-sestamibi during exercise and at rest. A dose of 370 MBq of ^99mTc-sestamibi was injected at the maximal level of exercise, and a myocardial image was obtained 90 min later (exercise image). Then, 740 MBq of ^99mTc-sestamibi was administered at rest, and myocardial imaging was repeated (rest image). The exercise and rest images were corrected for physical decay and injected doses, and the exercise image was subtracted from the rest image to obtain the corrected rest image. A response rate was calculated as follows: (exercise image - corrected rest image)×100/corrected rest image (%). The global response rates of 20 patients without significant coronary stenosis (≤50%) were higher than those of 67 patients with significant coronary stenosis (81 ±33% and 50±28%, p<0.01). Global response rates were correlated with the maximal rate pressure products during exercise (r=0.56, p<0.01) and delta rate pressure products (r=0.53, p<0.01). Regional response rates in myocardial areas perfused by stenotic coronary arteries of ≤50%, 75%, 90% and 99-100% were 60±24%,* 56±33%,* 40±23%* and 30±23%,* respectively, (*p<0.01 vs without significant coronary stenosis). The response rates decreased as the severity of coronary artery stenosis advanced, and distinguished between coronary stenoses of graded severity. Accordingly, the response rate from myocardial perfusion imaging with ^99mTc-sestamibi may provide complementary information to the conventional inspection with myocardial tomography regarding the severity of CAD. (Jpn Circ J 1998; 62: 592 - 598)

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The effects of L-158,809, an angiotensin II type 1 receptor antagonist, on cardiac hypertrophy and nephropathy were examined using Tsukuba hypertensive mice (THM) carrying both human renin and angiotensinogen genes. Nine male THM aged 20 weeks were assigned to each of a no-dosage group and an L-158,809 dosage group, and L-158,809 was administered for 8 weeks. Nine age-matched male C57BL/6 mice were used as normal control animals. At 28 weeks of age, all of the mice were euthanized. Systolic blood pressure, urinary volume, water intake volume, urinary albumin excretion, heart weight and kidney weight to body weight ratios and a glomerulosclerosis index were measured. In the no-dosage group, the values of all of these parameters were larger than those in the control mice. In the L-158,809 group, all of the parameters showed significant improvement, except for blood pressure, which was not significantly different from that in the no-dosage group. These results suggest that the renin-angiotensin system played a crucial role in the cardiac hypertrophy and nephropathy in THM, and that L-158,809 exhibited strong curative effects on cardiac hypertrophy and nephropathy by blocking the angiotensin II type 1 receptor. (Jpn Circ J 1998; 62: 599 - 603)

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Early-stage heart failure (HF) is characterized by an increase in circulating atrial natriuretic peptide (ANP) without activation of the renin-angiotensin-aldosterone system (RAAS) or body fluid retention. To test the hypothesis that elevated endogenous ANP suppresses the RAAS, maintains body fluid balance, and regulates vascular tone in early-stage HF, we assessed the effects of short-term and long-term inhibition of ANP on cardiorenal and neurohormonal functions. Short-term antagonism was produced by bolus administration (3 mg/kg) of HS-142-1, an antagonist of guanylate-cyclase coupled ANP receptors, and long-term antagonism was produced by continuous infusion (1 mg/kg per h) of HS-142-1 for 8 h to dogs with early-stage HF induced by rapid ventricular pacing (270 beats/min, 8 days). In this experimentally produced HF, plasma ANP was significantly increased relative to the pre-pacing value, but not plasma renin activity (PRA) or plasma aldosterone level. HS-142-1 significantly suppressed plasma and urinary guanosine 3', 5'-cyclic monophosphate (cGMP) levels, markers of endogenous ANP activity, in both experiments. Although mean arterial pressure and cardiac output did not change significantly, pulmonary capillary wedge pressure and right atrial pressure were elevated in both experiments. While short-term inhibition of ANP did not change PRA and aldosterone levels, long-term inhibition significantly increased these hormonal levels, resulting in decreases in urine flow rate, urinary sodium excretion rate, glomerular filtration rate, and renal plasma flow. These findings suggest that endogenous ANP plays a critical role in regulating venovascular tone, inhibiting activation of RAAS, and maintaining renal functions in early-stage HF. (Jpn Circ J 1998; 62: 604 - 610)

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To elucidate whether or not Ca channel blockers have an intrinsic benefit that cannot be attributed to the reduction of Ca²⁺ entry by pretreatment, time-averaged intracellular Ca²⁺ concentration ([Ca²⁺]_i) and energy-related phosphates were measured in isolated ferret hearts using nulear magnetic resonance. In the drug-free ischemic group, [Ca²⁺]_i increased significantly during 30 min of global ischemia at 30°C and during 0-5 min of reperfusion. After 30 min of reperfusion, isovolumic left ventricular developed pressure recovered only to 63±7% of the pre-ischemic level (mean ± SEM; N=5). Pretreatment with the Ca channel blocker clentiazem (10^-7 mol/L) itself depressed developed pressure by 53±9%. In the clentiazem group, [Ca²⁺]_i showed no significant changes during ischemia or reperfusion. Recovery of developed pressure (87±8% of untreated level) was significantly higher than in the non-treated group (p<0.05). Nevertheless, when the negative inotropism of clentiazem was offset by increasing [Ca]_o from 2 to 3 mmol/L, no beneficial effects of clentiazem were observed; [Ca²⁺]_i increased significantly during 0-5 min of reperfusion, and developed pressure recovered only 60±7% of untreated level. These results indicate that reduction of Ca²⁺ entry from the extracellular space to the myocyte, as reflected by negative inotropism during pretreatment, is required for clentiazem to protect myocardium in a model of global ischemia and reperfusion. (Jpn Circ J 1998; 62: 611 - 616)

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This report presents a 54-year-old woman with Goldenhar syndrome featuring an epibulbar dermoid, left microtia and a left preauricular appendage, and synostosis of the vertebrae. Multiple cardiovascular malformations including Wolff-Parkinson-White syndrome, a partial anomalous pulmonary venous connection, patent ductus arteriosus, an anomalous origin of the coronary arteries, and a right-sided descending aorta were revealed by electrocardiography, echocardiography and cardiac catheterization. Goldenhar syndrome is very rare, but the frequency of cardiovascular malformations in this syndrome is 5-58%. It is necessary to perform a careful evaluation of general malformations, especially cardiovascular malformations. (Jpn Circ J 1998; 62: 617 - 620)

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A patient with localized upper septal hypertrophy and medically uncontrolled severe outflow obstruction is described. His outflow obstruction was controlled by the implantation of a dual-chamber (DDD) permanent pacemaker. (Jpn Circ J 1998; 62: 621 - 622)

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A pacemaker was implanted into a 17-year-old man with cardiac failure due to complete atrioventricular block complicated by mitochondrial encephalomyopathy (Kearns-Sayre syndrome). Due to the possible complication of latent myocardial dysfunction, it was decided to implant the dual chamber pacemaker (DDD) and the operation mode was set to DDD 70 ppm 1 year after implantation; this alleviated the cardiac failure. In this case, the necessity of preventive pacemaker implantation in the early stage of cardiac failure was recognized. (Jpn Circ J 1998; 62: 623 - 625)

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A case is presented of endocarditis that was affecting a prosthetic ball valve (Starr-Edwards) and which was caused by Gemella species. A 57-year-old man was admitted with a 3-day history of abdominal pain with fever. At the time of admission, his temperature was 37.7°C and laboratory tests showed elevated inflammatory parameters and an increased neutrophil count. However, transthoracic echocardiogram showed no vegetation. During hospitalization, Gemella spp. were detected by blood culture, and a transesophageal echocardiogram showed vegetation on the prosthetic valve. He was treated with intravenous ampicillin and astromycin, and also underwent valve replacement. This is the first case in Japan of infective endocarditis of a prosthetic valve due to Gemella spp. (Jpn Circ J 1998; 62: 626 - 628)

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A case of exercise-induced idiopathic ventricular tachycardia (VT) arose from the left ventricular outflow tract. The QRS morphology of the VT was Rs pattern in V₁ and R pattern in the lateral leads with inferior axis. The pacing at the superior interventricular septum near the mitral anulus produced the best pace mapping. Radiofrequency application to this site suppressed the VT. (Jpn Circ J 1998; 62: 629 - 631)

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