Left main coronary trunk compression by dilated main pulmonary artery in atrial septal defect. Report of three cases.

Narrowing of the left main coronary trunk, which was compressed by the dilated pulmonary artery, was associated with atrial septal defect in three adults. One of them had severe pulmonary hypertension. Coronary angiograms revealed localized narrowing of the left main coronary trunk, and the left main coronary trunk had a concave shape. No stenosis of other coronary arteries was observed. In all patients the atrial septal defect was closed with a polytetrafluoroethylene patch. In the patient with 75% narrowing of the left main coronary trunk, aorta-coronary bypass was performed; it was not performed in the two with 50% narrowing. In two survivors postoperative coronary angiograms showed that the narrowing of the left main coronary trunk improved or disappeared. These results suggest that markedly dilated pulmonary arteries easily compress the left main coronary trunk and cause narrowing, which improves after atrial septal defect closure.

Contribution of calmodulin and protein kinase C to renin release in spontaneously hypertensive rats.

This study was designed to evaluate the contribution of calmodulin and protein kinase C to renin release from isolated glomeruli of spontaneously hypertensive rats (SHR, Okamoto and Aoki). Male 7-week-old SHR and age-matched control Wistar-Kyoto rats (WKY) were used in this study. Isolated glomeruli were sealed in the superfusion chamber and perfused with Krebs-Ringer solution at a constant flow of 0.3 mL/min. Renin release was increased by calmodulin inhibitor, W-7, and protein kinase C inhibitor, H-7, in both SHR and WKY. SHR showed higher maximal levels of renin release by W-7 and lower maximal levels by H-7 compared to WKY. These results indicate that calmodulin and protein kinase C play inhibitory roles in renin release from juxtaglomerular cells. The calmodulin-mediated suppression mechanism in renin release appears to be augmented in the SHR, whereas the protein kinase C-mediated system is attenuated.

Pheochromocytoma-related myocardial damage following delivery.

We present the case of a 35-year-old woman whose pregnancy was complicated by the rare condition of transient pheochromocytoma-related myocardial damage. Short-duration left ventricular dysfunction was apparently caused by acute non-transmural myocardial infarction provoked by coronary artery vasospasm rather than catecholamine-induced cardiomyopathy. Forty-eight days after onset, a 50 x 55 x 35 mm tumor was excised and histologically confirmed to be a pheochromocytoma.

Abnormal heart rate control in vasospastic angina: effects of calcium antagonists.

We examined the effects of administration of calcium antagonists on the heart rate response to treadmill exercise in 11 patients with vasospastic angina and 8 healthy young volunteers. The exercise test was performed by walking on a treadmill at a constant speed and grade according to a scheme of pseudo-randomized sequence for 19 min. The dynamic property of heart rate response to exercise was evaluated by using a frequency analytic procedure. The exercise test was also studied in 21 age-matched normal controls without drug administration. Administration of calcium antagonists revealed no significant effects on heart rate and blood pressure at rest in young healthy subjects or in patients with vasospastic angina. Young volunteers showed the same normal properties of heart rate response to exercise before and after calcium antagonists. Vasospastic angina showed abnormal heart rate response to exercise and revealed characteristically different transfer function from that in normal controls. These characteristics were not affected by treatment with calcium antagonists except for a slight, uniform decrease of gain of the system over the whole frequency range. Accordingly, the present exercise test can feasibly be used in the diagnosis and management of vasospastic angina even when calcium antagonists are administered to the patients.

Poor responsiveness of heart rate to treadmill exercise in vasospastic angina.

Heart rate response to submaximal graded treadmill exercise was measured in 45 patients with vasospastic angina, 31 with effort angina, and 40 normal controls. There was no difference of resting heart rate among the three groups. Vasospastic angina showed significantly poor responsiveness of heart rate to exercise at every stage: stage 1, 2.5 km/h (10%), stage 3, 4.5 km/h (10%), stage 5, 5.5 km/h (14%), stage 7, 5.5 km/h (22%), when compared with those in normal controls. The effort angina group also showed lower heart rates at stages 3 and 5 than those in control subjects, although their heart rate at stage 1 was not different from that in normals. When abnormal response suggesting vasospastic angina was defined as heart rate at each stage lower than values of mean heart rate +/- 1 SD in normal controls, positive test results were obtained in 15 of 45 patients (33%). The use of heart rate criteria in addition to ischemic criteria raises sensitivity from 27 to 51% (p less than 0.02).

Diagnosis of vasospastic angina by analysis of heart rate response to exercise: effects of different levels of work load.

To examine alterations in control functions of the heart, which may account for the pathophysiologic conditions precipitating coronary arterial spasm, heart rate response to exercise in vasospastic angina was evaluated by using our previously developed method of frequency analysis. We also examined the effects of three different levels of work load on the heart rate response to treadmill exercise in 9 patients with vasospastic angina and 7 normal controls: stage 1 (2.5 Km/h, 10%), stage 3 (4.5 Km/h, 10%), and stage 5 (5.5 Km/h, 14%). The transfer function of heart rate control in vasospastic angina was characteristically different from that in normal controls: lower gain and more delayed phase angle of the system. Although this abnormality was observed in every test at 3 different levels of work load, the abnormality was more striking in tests at lower levels of work load: stage 1 or 3. The moderately light exercise test at stage 3 is most suitable as a test for detecting abnormal heart rate response to exercise in vasospastic angina because the exercise test at stage 1 had a poor S/N ratio.

[Long-term prognosis related to coronary risk factors, clinical characteristics of acute myocardial infarction and coronary angiographic findings in the elderly].

In order to clarify the characteristics of acute myocardial infarction in the elderly, we investigated the clinical profile and long-term prognosis of patients with myocardial infarction in the past 13 years. The early fatality rate (within 30 days after onset) in the relatively younger patients (less than 65 years old) was 8.8%, and in the older patients (greater than 65 years old) was 29.1%. The fatality rate was significantly higher in older than in younger patients. On coronary and left ventriculography, the older patients showed multi-vessel lesions with decreased ejection fraction and cardiac index. According to the cumulative survival curves related to the coronary risk factors, no significant differences were found with or without smoking or hypertension. However, the long-term prognosis of the patients with controllable hypercholesteremia was better than in uncontrollable patients less than 65 years old. No significant difference was found in patients with hypercholesteremia over age 65. The long-term prognosis of the patients with uncontrollable diabetes mellitus was worse than that of controllable diabetic patients.

Effects of locally administered argatroban on restenosis after balloon angioplasty: experimental and clinical study.

1. This study was undertaken to evaluate the preventive effects of locally administered argatroban, a competitive inhibitor of thrombin-induced platelet activation, on restenosis after balloon angioplasty. 2. A hydrogel-coated balloon catheter was immersed three times in argatroban/saline solution (1 mg/mL) for 60 s, inflated to a pressure of 606 kPa and left in the rabbit common carotid artery for 1 min. The same procedure was performed, without drug, as a control. The pharmacokinetics of delivered argatroban in the arterial wall were assessed using [14C]-argatroban. Platelet deposition 2 h after balloon injury was quantified by fluorescence studies using antiplatelet antibody. Vascular smooth muscle cell (VSMC) proliferation 3 days after balloon injury was assessed by immunohistochemical staining for proliferative cell nuclear antigen (PCNA). In a clinical study, we divided 50 elective patients into two groups: argatroban and control. 3. In the experimental study, the mean quantities of argatroban at 0, 2 and 6 h after deflation were 24.63, 0.49 and 0.11 nmol/g wet weight of artery, respectively. Argatroban was undetected 24 h after deflation. Two hours after deflation, argatroban-treated arteries showed less platelet adhesion than saline-treated controls. The mean number of PCNA-positive cells was 16.9 and 43.8% in the argatroban and control groups, respectively (P < 0.01). In the clinical study, the mean late gain loss was 8.2 and 27.3% in the argatroban and control groups, respectively (P < 0.05). The mean late restenosis rate was 11.1 and 41.4% in the argatroban and control groups, respectively (P < 0.05). 4. These data suggest that blood coagulation plays a significant role in VSMC proliferation after balloon injury and that locally administered argatroban using hydrogel-coated balloon catheter may prevent post-percutaneous transluminal coronary angioplasty restenosis.

Effects of locally administration of argatroban using a hydrogel-coated balloon catheter on intimal thickening induced by balloon injury.

The purpose of this study was to evaluate the inhibitory effects of locally delivered argatroban, a competitive inhibitor of thrombin-induced platelet activation, on intimal proliferation after balloon injury. A hydrogel-coated balloon catheter was immersed 3 times in an argatroban/saline solution (1, 0.1, or 0.01 mg/ml) for 60 s and inflated at 6 atm pressure for 1 min in the rabbit common carotid artery. Immersion in a saline solution without drug followed by the same procedure served as a control. Accumulation of argatroban in the vascular wall was confirmed by chemical determination using high-performance liquid chromatography (HPLC). The concentration of argatroban in the vessel wall immediately after deflation after balloon immersion in solutions of 1 and 0.1 mg/ml was 14.8 +/- 10.9 and 5.5 +/- 4.6 nmol/g wet weight of artery, respectively. Argatroban was not detected in arteries treated with a balloon that had been immersed in the 0.01 mg/ml argatroban/saline solution. Intima-media area ratios 20 days after balloon injury in the groups treated with 1 mg/ml (n = 8) and 0.1 mg/ml (n = 6) agratoban were significantly smaller than that in the groups treated with 0.01 mg/ml (n = 7) argatroban or saline (n = 8) (0.35 +/- 0.11, 0.50 +/- 0.17, 1.24 +/- 0.39, and 1.35 +/- 0.43, respectively; p < 0.001). These data suggest that locally administered argatroban dose-dependently inhibits intimal thickening in a rabbit model of carotid artery injury.

[Assessment of right ventricular function by magnetic resonance imaging of old myocardial infarction].

The usefulness of magnetic resonance imaging (MRI) for estimating right ventricular function and the influence of left ventricular dysfunction on the performance of the right ventricle were assessed in 43 patients with chronic myocardial infarction (MI) and 14 control subjects (N) using electrocardiography-gated MRI and cardiac catheterization. Patients with MI were divided into three groups according to the location of the coronary lesions; 22 patients with left coronary artery lesion (LCA group), 13 with right coronary artery lesion (RCA group), and 8 with both left and right coronary artery lesions (L+R group). The right ventricular end-diastolic volume (RVEDV) and right ventricular ejection fraction (RVEF) were measured by Simpson's rule algorithm on transverse images of the right ventricle obtained at the end-systolic and end-diastolic phases. In 34 of the 43 patients, the same parameters of right ventricular function were calculated by the thermodilution method using a Swan-Ganz catheter with rapid response thermistor. Left ventricular ejection fraction (LVEF) and end-diastolic volume were determined from left ventriculography. The intraobserver reproducibility (11 cases, r = 0.97) and interobserver reproducibility (11 cases, r = 0.92) of RVEF measured by MRI were excellent. The RVEF and RVEDV determined from MRI were significantly correlated with those from the thermodilution method (RVEF: r = 0.56, RVEDV: r = 0.52). There was no difference in right ventricular end-diastolic volume index in any patient group. The RVEF was decreased in the L+R (41.0 +/- 4.5%, p < 0.01) and RCA (45.9 +/- 6.6%) groups, but there was no difference between the LCA (50.6 +/- 6.6%) and N (48.9 +/- 4.3%) groups.(ABSTRACT TRUNCATED AT 250 WORDS)

A premenopausal woman presenting with acute myocardial infarction of three different coronary vessels within 1 year: role of lipoprotein(a).

A premenopausal female patient presented with acute myocardial infarction of 3 different coronary vessels at different times within 1 year. These events were caused not by restenotic lesions after balloon angioplasty but by new lesions, which were successfully treated by primary angioplasty. Although she had a history of hypertension, type IIB hyperlipidemia, and diabetes, they had been well-controlled on medication. An elevated serum lipoprotein(a) level may have played a role in this rapid angiographic progression.

Dynamic outflow obstruction due to the transient extensive left ventricular wall motion abnormalities caused by acute myocarditis in a patient with hypertrophic cardiomyopathy: reduction in ventricular afterload by disopyramide.

A 65-year-old woman was admitted to the coronary care unit because of acute pulmonary edema. Immediate 2-dimensional and Doppler echocardiograms revealed extensive left ventricular wall motion abnormalities and left ventricular hypertrophy with extreme outflow obstruction. Although an ECG showed ST-segment elevation in the anterolateral leads, a coronary arteriogram revealed normal epicardial arteries. Heart failure was relieved after diminishing the dynamic outflow obstruction with disopyramide administration. An endomyocardial biopsy from the right ventricle on the 8th hospital day showed borderline myocarditis. Wall motion abnormalities gradually normalized within 2 weeks. It is speculated that her pulmonary edema would not have been relieved so readily without the immediate reduction in ventricular afterload by disopyramide. These clinical changes over time were observed with serial echo-Doppler examinations.

The cause of death, risk factors and long-term prognosis of acute myocardial infarction.

Three hundred and eighty-six patients with acute myocardial infarction in the past 11 years between 1975 and 1985 were investigated retrospectively to clarify fatality, cause of death and long-term prognosis in relation to their risk factors and age. The average number of patients admitted in each year was 24.4 for the first 5 years and 44.0 cases per year in the last 5 years. The fatality decreased from 20.3% in the first 5 years to 15.7% in the last 5 years. A major cause of hospital death was cardiogenic shock and congestive heart failure. One hundred and thirty-six patients had coronary arteriography within 2 months after admission. They were divided into three groups; the young (less than or equal to 40 year old)-, middle (41-50 year old)-, and old (greater than or equal to 51-year old)-aged groups. Among the young-aged group, serum cholesterol levels at admission were significantly higher in patients with multi-vessel lesions than those in patients without multi-vessel lesions, while there were many heavy smokers who did not show a significant lesion of the coronary artery. These observations suggest that hypercholesterolemia may act as an important risk factor for coronary arteriosclerosis in young patients, and also that a heavy smoking may promote an initiation of myocardial infarction in young patients without severe coronary artery stenosis. The cumulative 5 and 10 year survival rate for all groups was 84% and 61%, respectively. Fifty-seven patients had reinfarctions, and thirty patients died. The survivors were younger and had a good tolerance to treadmill exercise test at discharge.

[Change in argatroban concentration within the vessel wall after local administration using hydrogel-coated balloon catheter].

Acute coronary occlusion after percutaneous transluminal coronary angioplasty is one of the major problems in coronary intervention. This study evaluated the hydrogel-coated balloon delivery of argatroban to the arterial wall and argatroban persistence after angioplasty in 17 rabbits. A hydrogel-coated balloon was immersed three times in argatroban/saline solution (1 mg/ml) and inflated at 6 atm pressure for 1 min in the common carotid artery. The transfer of argatroban to the vascular wall was measured by high-performance liquid chromatography. The concentrations of argatroban at 0, 5, and 15 min after deflation were 14.8, 4.2, and 3.9 nmole/g.wet weight. The hydrogel-coated balloon catheter can deliver argatroban to the local arterial wall during balloon inflation.

[Lesion-related factors associated with restenosis after percutaneous transluminal coronary angioplasty in the absence of patient-related factors].

Restenosis after percutaneous transluminal coronary angioplasty (PTCA) is one of the biggest problems in the treatment of coronary artery disease. Although many studies have been performed on lesion-related factors, they are influenced by patient-related factors such as smoking, hyperlipidemia, and the presence of acute coronary syndrome. In this study, lesion-related factors were assessed in the absence of other factors by univariate and multivariate analysis. One hundred and nine lesions were reviewed in 37 consecutive patients with both restenotic lesion(s) and non-restenotic one(s) confirmed by coronary arteriography performed 4.4 +/- 2.2 months after PTCA. Angiographic findings before and immediately after angioplasty were compared between restenotic and non-restenotic lesions. The overall lesion-restenosis rate was 42%. Univariate analysis revealed that calcified lesions (p < 0.05), multiple irregularities (p < 0.01) before angioplasty, residual percentage stenosis (p < 0.05), and angiographical intraluminal haziness (p < 0.05) were related to restenosis. Intimal dissection after PTCA was not associated with restenosis. Multivariate analysis with multiple logistic regression revealed that multiple irregularities (t = 2.8) was the most predictive of restenosis before PTCA and residual percent stenosis (t = 2.6) after the procedure. Coronary lesions with calcification or multiple irregularities indicate high risk of restenosis after PTCA. Optimal dilatation of the lesions without intraluminal haziness regardless of intimal dissection is important to prevent restenosis.

[Magnetic resonance imaging of coronary artery lesions using modified spin-echo sequence].

Magnetic resonance imaging of the cardiovascular system has been beset with difficulties in obtaining clear images due to prominent artifacts which course in the direction of the phase encoding axis. These artifacts are commonly believed to derive from blood flow. However, in the ECG-gated spin-echo (SE) sequence using two-dimensional Fourier transform reconstruction, variation in effective repetition time due to physiological changes in the R-R interval of ECG may also result in prominent artifacts. To eliminate these artifacts, we developed a new method, the modified spin-echo (MSE) sequence, by adding a nonselective 90 degree radio-frequency pulse and an optional delay time (Td) prior to the conventional SE sequence. In the MSE sequence, artifacts derived from the cardiovascular system were markedly suppressed. Using the MSE sequence, we attempted direct imaging of the coronary vessels, and obtained very clear images of the coronary arteries and veins. Organic lesions in the coronary arteries were also clearly imaged, including coronary stenosis, dilatation, coronary fistulae, and abnormality of the origin of the right coronary artery. The MSE sequence may offer a clinical advantage in obtaining coronary artery images, and may be used to evaluate coronary artery disease.

[Echocardiographic features of left ventricular hypertrophy and contractility in malignant hypertension].

To assess the hemodynamic characteristics in malignant hypertension, echocardiography was performed in 18 patients with malignant essential hypertension (MH-I, n = 9) and secondary hypertension (MH-II, n = 9). Patients with benign hypertension with or without left ventricular hypertrophy (n = 8 and 7, respectively), patients with hypertensive heart failure (n = 7) and normotensive volunteers (n = 10) were subjected to controls. Plasma noradrenaline (NA) and renin activity (PRA) were also measured prior to the antihypertensive therapy. There were no significant differences in the durations of hypertension before the malignant phase, and the mean arterial pressure between MH-I and MH-II. Although posterior wall thickness (PWTd) in MH-II was similar to that in MH-I, interventricular septal thickness (IVSTd) was less marked in MH-II. The plasma NA and PRA were markedly increased in both MH-I and MH-II. End-diastolic dimension (Dd) of the left ventricle was within normal range, but end-systolic dimension (Ds) was significantly increased in MH-I, MH-II and hypertensive heart failure. The moderate decreases in ejection fraction (EF) and mean velocity of circumferential fiber shortening (mVcf) were observed in both MH-I and MH-II. Marked decreases in EF and mVcf were also observed in patients with hypertensive heart failure. The relationship between systolic blood pressure and Dd/PWTd was shifted toward the right and upper portion of the normal relation in MH-I and MH-II. The present study demonstrated that the hemodynamic characteristics in malignant hypertension are an inappropriate left ventricular hypertrophy due to a marked increase in systolic stress; dilatation of the left ventricle in systole; and a moderate decrease in ventricular systolic function. It is suggested that a decrease in left ventricular systolic function in malignant hypertension might be due in part to a marked increase in the influence of neurohumoral factors on hemodynamics.