Effects of therapeutic doses of human atrial natriuretic peptide on load and myocardial performance in patients with congestive heart failure.

The benefits of atrial natriuretic peptide (ANP) in patients with congestive heart failure (CHF) have been demonstrated. However, the myocardial actions of ANP remain unclear. Using relatively load-insensitive left ventricular pressure-volume analysis, the myocardial and load-altering actions of ANP in patients with moderate CHF were studied. After obtaining steady-state data using micromanometers and conductance catheters, ANP was infused in 9 patients with CHF at 0.01 and 0.1 microg/kg/min for 30 minutes, respectively. Hemodynamic variables, plasma ANP, and cyclic guanosine monophosphate (cGMP) levels were determined before and 30 minutes after each ANP infusion. ANP at 0.01 microg/kg/min increased plasma ANP and cGMP levels from 73 +/- 34 to 139 +/- 34 pg/ml and from 4 +/- 1 to 8 +/- 2 pmol/ml, respectively. ANP infusion caused a significant decrease in end-systolic pressure without any changes in heart rate. End-diastolic pressure was significantly decreased but there was no significant change in left ventricular end-diastolic volume. The time constant for isovolumetric relaxation was decreased. ANP infusion at 0.1microg/kg/min caused further decreases in end-systolic pressure, end-diastolic pressure and volume, and the time constant for isovolumetric relaxation (p <0.05) without any changes in heart rate. The slope of the end-systolic pressure-volume relation was increased from 1.3 +/- 0.2 to 1.6 +/- 0.3 mm Hg/ml (p <0.05), indicating increased contractility. Plasma ANP and cGMP levels were increased to 422 +/- 44 pg/ml and 16 +/- 3 pmol/ml, respectively. Thus, ANP infusion increased cGMP generation, decreased afterload and preload, and improved left ventricular systolic and diastolic function.

[A case of stunned myocardium with marked 99mTc-PYP accumulation].

A 71-year-old woman with unstable angina was admitted to our department. Upon admission, electrocardiography revealed a QS pattern in Leads V1-V3. Left ventriculography disclosed akinesis of the anterior wall and the septum. Myocardial scintigraphy with 99mTc-pyrophosphate (PYP) revealed marked accumulation (Parkey's grade III) in the anterior wall, septum and apical region. Coronary arteriography revealed stenosis (99% with delay) in the LAD #6. Based on these findings, we performed percutaneous transluminal coronary angioplasty (PTCA) on this patient. About 3 months later, the patient underwent PTCA again because stenosis had recurred. The resting 201Tl myocardial scintigram, taken immediately after the first PTCA, demonstrated complete defects in the anterior wall, septum and apical region. After the second PTCA, no stenosis was observed. About 1 year later, the wall motion returned to normal (except in part of the apical region), suggesting that this was a case of stunned myocardium. On the same occasion, the 201Tl uptake was normal except in the apical region. The present case was regarded as stunned myocardium which demonstrated marked radioactivity accumulation when examined by 99mTc-PYP myocardial scintigraphy. In the past, 99mTc-PYP has been thought to be incorporated into irreversibly impaired myocardium (e.g., in cases of acute myocardial infarction). The uptake of 99mTc-PYP into stunned myocardium has not been reported before. Thus, this case is rare and noteworthy.

[A case of congenital long QT syndrome associated with T wave alternans].

A case was presented in which a rare T wave alternans occurred in association with congenital long QT syndrome. A 71-year-old woman, who had experienced several syncopal attacks per year for the previous forty years, was admitted for further evaluation of the syncope. She had a family history of sudden death (sister) and QT prolongation (son). Electrocardiogram showed a corrected QT interval of 0.68 seconds. Treadmill exercise-tolerance test revealed both T wave alternans immediately after exercise and torsades de pointes 150 seconds after exercise. The syncope was induced by the mental excitation. A prolonged corrected QT interval reduced from 0.70 seconds to 0.58 seconds by the correction of her serum potassium and magnesium. The effect of propranolol, verapamil, phenytoin or mexiletine on T wave alternans and ventricular arrhythmia was evaluated by the treadmill exercise-tolerance test. The treatment with propranolol was most effective.

[Exercise-induced left bundle branch block in treadmill exercise test: clinical significance and prognosis].

Exercise induced left bundle branch block (LBBB) is poorly understood. We investigated its clinical characteristics and prognosis. The records of 3,459 consecutive patients who underwent treadmill exercise testing were reviewed. Exercise induced LBBB was identified in 6 patients (0.17%). Three out of six patients had underlying cardiac disease; two had coronary artery disease and one dilated cardiomyopathy. Three out of five had redistribution on Tl-201 myocardial scintigraphy. In one of these three patients, however, coronary angiography demonstrated no significant narrowings. Tl-201 myocardial scintigraphy in patients with exercise induced LBBB may be undetermined for coronary artery disease. During follow-up, one of six patients had depressed left ventricular function and was diagnosed as having dilated cardiomyopathy. It is thus obvious that exercise induced LBBB without a specific underlying heart disease should be followed up carefully.

[Influence of Lp(a) on restenosis after coronary angioplasty].

We clarified the relationship between lipoprotein (a) concentration and restenosis after coronary angioplasty (PTCA). The lipoprotein (a) concentration in patients with restenosis after PTCA was significantly higher than in patients without restenosis after PTCA (33.0 +/- 19.8 mg/dl vs 19.1 +/- 17.4 mg/dl, p less than 0.05]. Moreover, patients with a lipoprotein (a) concentration of more than 30 mg/dl had a high rate of restenosis after PTCA. Restenosis after PTCA is related to lipoprotein (a) concentration.

Multiple pulmonary emboli with pulmonary hypertension caused by effort thrombosis and effective balloon venoplasty of the subclavian vein.

A 36-year-old woman with effort thrombosis of the subclavian vein associated with multiple pulmonary emboli was successfully treated with local thrombolysis of the subclavian vein using a pulse-spray catheter and systemic anticoagulation. Balloon venoplasty of the residual stenosis of subclavian vein was carried out and in follow-up venography 6 months later, there was no restenosis, and the patient has been asymptomatic for 12 months. Pulmonary embolism is not a rare complication of upper extremity deep vein thrombosis and should be managed as aggressively as lower extremity deep vein thrombosis.

Ischemic heart disease showing unusual angiographic findings.

Atherosclerotic lesions usually occur in the proximal and middle portion of the coronary arteries. Multiple obstructive lesions appearing only in the peripheral branches without lesions in the proximal or distal portion have not been reported. We encountered a patient with ischemic heart disease showing multiple obstruction in the peripheral branches of the right and left coronary arteries without significant stenotic lesions in the proximal or middle portion. This 49-year-old male was admitted to Yamada Red Cross Hospital due to angina pectoris. Coronary risk factors for him included hypertension, abnormal glucose tolerance, smoking habit, and obesity. Laboratory studies showed a complete blood count and normal blood chemistries, as well as thromboplastin and prothrombin times. Coronary angiography showed multiple obstruction or marked stenosis in the distal portion and peripheral branches; there was no stenosis in the proximal and middle portions. Left ventriculography showed severe hypokinesis in the diaphragmatic segment. Biopsy of the left ventricular endocardium showed interstitial fibrosis but showed no abnormalities in the myocardial fibers or cell infiltration to perivascular areas and vascular walls. Coronary angiography after two months showed multiple lesions, as previously observed. Although ischemic heart disease is caused by various types of vasculitis, embolism, coronary spasm, and fibromuscular dysplasia, in this patient, there were no findings suggestive of causes other than atherosclerosis. This case is interesting in terms of rare angiographic findings and its cause.

A case of dilated cardiomyopathy manifested by exercise-induced left bundle branch block.

We report an extremely rare case of dilated cardiomyopathy manifested by exercise-induced left bundle branch block. A 63-year-old female came to our hospital because supraventricular arrhythmia had been detected at a check-up. A treadmill exercise test induced left bundle branch block. However, chest X-ray and echocardiography revealed no abnormal finding. Two years later, the patient experienced exertional dyspnea. A chest X-ray examination showed cardiomegaly, and echocardiography showed a moderate impairment of left ventricular function with left ventricular dilatation. The diagnosis of dilated cardiomyopathy was made by left ventricular myocardial biopsy. No previous cases have initially shown exercise-induced left bundle branch block which was followed by left ventricular dysfunction due to dilated cardiomyopathy. Careful long-term observation of the clinical course is necessary in patients with exercise-induced left bundle branch block which shows no significant underlying disease.