Effects of direct percutaneous transluminal coronary angioplasty treatment of acute myocardial infarction on plasma levels of haemostatic and fibrinolytic factors.

Although thrombolytic therapy is used widely for treatment of acute myocardial infarction (AMI), thrombolysis itself increases thrombin activity and may cause reocclusion of infarct-related vessels. Direct percutaneous transluminal coronary angioplasty (PTCA) is an effective treatment for AMI; however, it is not clear what effects PTCA has on coagulation and fibrinolysis. We investigated coagulation and fibrinolytic factor concentrations before and after direct PTCA. Plasma levels of thrombin-antithrombin III complex (TAT), D-dimer, plasmin-(alpha 2-antiplasmin complex (PAP), tissue-type plasminogen activator (t-PA) antigen and plasminogen activator inhibitor (PAI)-1 antigen were followed in twelve patients treated with direct PTCA for AMI. Before PTCA, only TAT concentrations were significantly elevated compared to normal controls. D-dimer, TAT, PAP and PAI-1 concentrations were similar before and after PTCA. Eleven patients had no recurrent ischaemia and no restenosis on follow-up coronary angiography. These data confirm that direct PTCA is less likely than thrombolysis to affect coagulation and fibrinolysis.

[Two cases of coronary artery-left ventricular fistula associated with left ventricular hypertrophy].

Two cases of coronary artery-left ventricular fistula (AVF) associated with left ventricular hypertrophy were reported. The first patient was a 53-year-old man with chest pain. Selective coronary angiography (CAG) revealed bilateral coronary arteries draining into the left ventricle (LV). The second patient was a 46-year old man with electrocardiographic (ECG) abnormalities. CAG showed bilateral coronary artery which communicated via a maze of fine vessels into LV. In both cases, ECG showed ST depression and inverted T wave, and two-dimensional echocardiography revealed hypertrophic cardiomyopathy (HCM). Coexistence of coronary artery-left ventricular fistula and HCM seems to be a casual association.

Reflex control of atrioventricular nodal refractory periods by cardiopulmonary receptors in humans.

The effects of selective cardiopulmonary receptor unloading on atrioventricular (AV) conduction were examined in 7 patients undergoing electrophysiologic testing. During -35 mmHg lower body negative pressure (LBNP) before autonomic blockade with propranolol and atropine, the AV-nodal conduction time (AH interval), the effective and functional refractory periods of AV node decreased at paced cycle length, when systemic arterial and central venous pressures decreased and heart rate increased. These responses to -35 mmHg LBNP except reductions in systemic arterial and central venous pressures disappeared after autonomic blockade. During -10 mmHg LBNP before autonomic blockade, both effective and functional refractory periods of AV node at paced cycle length decreased by 11 +/- 3% (mean +/- SEM) and 6 +/- 1% respectively with the reduction of central venous pressure while AH interval, systemic arterial pressure and heart rate remained unchanged. After autonomic blockade, -10 mmHg LBNP reduced central venous pressure but all the other parameters remained unchanged. These results suggest that cardiopulmonary baroreceptors participate in the reflex control of AV nodal refractoriness in humans.

[Abnormal left ventricular flow during diastole in hypertrophic heart disease].

This study was performed to investigate the characteristics of isovolumic relaxation flow velocity (IRFV) in the mid-portion of the left ventricle. Doppler examinations were performed at rest in 20 subjects with normal heart and 18 with hypertrophic heart disease. To assess the left ventricular flow conditions in hyperdynamic states, 10 healthy subjects underwent exercise Doppler echocardiography. From the apical transducer position, left ventricular filling velocities were obtained at the mitral valve orifice level and at the mid-ventricle, and the changes of peak velocities in the rapid filling (R0, R1) and atrial contraction phases (A0, A1) were measured [%R = (R1-R0)/R0, %A = (A1-A0)/A0]. There was a good correlation between IRFV and %R (IRFV = 0.69 X %R + 25.9, r = 0.75, p less than 0.001). However, there was no correlation between IRFV and %A. Prominent IRFV (greater than or equal to 30 cm/sec) was demonstrated in 13 subjects, including 10 with hypertrophic heart disease. During exercise, IRFV, %R and %A did not increase. It was concluded that a prominent IRFV was associated with the acceleration of rapid filling velocity at the mid-ventricle. This phenomenon may be caused by regional and asynchronous hyperdynamic states demonstrated in hypertrophic heart disease.

Transient ST-segment elevation in subarachnoid hemorrhage.

Electrocardiographic manifestation mimicking the hyperacute phase of myocardial infarction and the electrical alternans of the elevated ST-segment in association with subarachnoid hemorrhage were reported in two patients with no evidence of heart disease. In both cases the ST-segment changes were transient and there were no persistent changes suggestive of underlying myocardial damage or ischemia. These findings suggested that the electrocardiographic changes were probably secondary to subarachnoid hemorrhage and not an expression of primary myocardial disease. The electrocardiographic abnormalities could be explained by altered autonomic activity to coronary arteries or directly to the myocardium.

Acute renal failure secondary to rhabdomyolysis associated with dissecting aortic aneurysm.

Rhabdomyolysis, a massive necrosis of skeletal muscle, is caused by various traumatic and non-traumatic factors. We report on a 30-year-old male in whom dissecting aortic aneurysm diagnosed by computed tomography was responsible for the generation of rhabdomyolytic acute renal failure. The patient was successfully treated by repeated hemodialyses and corrective surgery for aortic regurgitation and dissecting aortic aneurysm (Bentall's operation).

[Respiratory changes of superior vena cava flow velocity in old myocardial infarction with severe left ventricular dysfunction].

The clinical significance of the flow velocity of the superior vena cava (SVC) in old myocardial infarction (OMI) with severe left ventricular dysfunction were evaluated using pulsed Doppler echocardiography. The subjects consisted of 10 patients with OMI (averaged left ventricular ejection fraction: 0.37 +/- 0.11) and 10 age-matched normal controls. Among the patients, eight had extensive anterior infarction and two had both anterior and inferior infarctions. During normal respiration, the peak SVC flow velocities in systole (S) and diastole (D), and the D/S ratio were measured. To evaluate right ventricular diastolic function, we measured the peak velocity across the tricuspid orifice in early diastole (rapid inflow: T-R) and the atrial contraction phase (T-A), and the ratio T-A/T-R during quiet expiration. In the normal controls, S was greater than D, both during expiration and inspiration. During inspiration, S, D and the D/S in the normal controls increased, with a greater increase in D than in S. In the patients, however, D and the D/S did not increase during inspiration. T-R was less and the T-A/T-R was greater in the patients with OMI than in the normal controls. These findings of tricuspid flow velocity revealed impaired diastolic filling of the right ventricle in patients with OMI. In conclusion, the impaired diastolic filling of the right ventricle in patients with OMI might be one of the causes of the abnormal response of the SVC flow velocity during normal spontaneous respiration.

Primary hemangiopericytoma of the heart associated with pseudoaneurysm of the pulmonary artery--a case report.

A thirty-three-year-old male with malignant hemangiopericytoma of the right ventricular outflow tract and the pulmonary artery associated with pseudoaneurysm formation at the latter is presented. Contrast computed tomography was helpful in diagnosing the pseudoaneurysm of the pulmonary artery. The positional change of the murmur, with a tumor plop caused by the pedunculated tumor of the right ventricular outflow tract, was detected.

[Malignant hemangiopericytoma of the right ventricular outflow tract and the pulmonary artery: a case report].

A case of malignant hemangiopericytoma of the right ventricular outflow tract and the pulmonary artery associated with formation of a pseudoaneurysm in the latter is presented. This 33 year-old man had a four month history of illness. From the surgical point of view, all non-invasive modalities including phonocardiography, M-mode and two-dimensional echocardiography, radionuclide angiocardiography and contrast computed tomography underestimated the extent of the tumor as compared with the selective cineangiographic estimation. Therefore, it was suggested that in some situations where surgery is contemplated, a combination of non-invasive methods and cineangiography is essential to obtain sufficient diagnostic information, although the introduction of catheters into the right-sided cardiac chambers containing a mass might be hazardous because of potentiality dislodging portions of a tumor or adherent thrombus. Concerning pericardial abnormalities, contrast computed tomography was the most sensitive and specific method among the diagnostic techniques used in this case.

Electrophysiologic effects of diltiazem, a calcium antagonist, in patients with impaired sinus or atrioventricular node function.

The electrophysiologic effects of diltiazem, a calcium antagonistic agent, were studied in 30 subjects with various degrees of sinus or AV node dysfunction. After diltiazem was administered, sinus activity was not depressed in control subjects, whereas marked inhibition was observed in some of the patients with sick sinus syndrome. Ventricular automaticity was little affected by this drug. The AV conduction system was significantly depressed, and there was no difference in degree between controls and AV block patients. The depression of the AV conduction system became more marked as the basic atrial cycle length was shortened. The drug had no apparent effects on atrial refractoriness, atrial echo zone, or the accessory pathway system. Conclusively, diltiazem affects mainly sinus and AV conduction systems. Its effect on the sinus mode may provide a hazardous problem in patients with the sick sinus sysdrome patients, while its effect on the AV node will have therapeutic value in patients with AV nodal re-entrant arrhythmias.

[Therapeutic significance of controlling heart rate in aortic regurgitation (author's transl)].

The hemodynamic effects of aortic regurgitation are characterized by an increase of left ventricular volume load due to the diastolic regurgitation and a decrease of aortic diastolic pressure or coronary perfusion pressure. It is presumed that an increase of heart rate in such a situation diminishes the regurgitant flow and elevates the coronary perfusion pressure so far as it is not accompanied by an improper increase of myocardial oxygen consumption. The present study, although it was the one performed on dog heart with an aortoventricular shunt rather than aortic valvular destruction, demonstrated that the increase of heart rate, if not beyond 160 beats per min, minimizes regurgitant flow as well as regurgitant ratio and maintains effective cardiac output without impairing coronary circulation. Thus it is suggested that it would be of beneficial therapeutic means in aortic regurgitation to keep the heart rate high or, at least, to avoid its excessive deceleration.

Changes of cardiac performance in renal failure.

Clinical and experimental studies were carried out in order to evaluate the role of myocardial dysfunction in the genesis of circulatory congestion associated with renal failure. Among the patients with chronic renal failure, those with circulatory congestion had greater blood volume and higher venous pressure while lower cardiac index and stroke work index than those without circulatory congestion. After peritoneal dialysis, although blood volume and venous pressure decreased in both groups, cardiac index increased in the former while it decreased in the latter group. In 15 dogs, acute renal failure was produced by ligating both ureters. As uremia developed, blood volume and left ventricular end-diastolic pressure increased with or without an increase in cardiac index. The depression of ventricular function curve was evident in all the dogs. The peritoneal dialysis performed at this stage resulted in a prompt recovery of left ventricular end-diastolic pressure with minimum change in cardiac index. The measurement of dp/dt/IIT also indicated a depression of myocardial contractility at uremic stage and its recovery after dialysis. We conclude that impairment of myocardial function is implicated in the development of circulatory congestion in renal failure.