Forty years ago, after the establishment of coronary care units, a significant decrease in mortality of acute myocardial infarction was noted. Twenty years ago, the break-through of thrombolysis realized once again a significant decrease in mortality. In this study we compare, in a rather small community hospital, the mortality and safety of thrombolytic therapy in acute myocardial infarction with a more conventional, conservative medical therapy.
We examined all cases of acute myocardial infarction between 1978 up to 1998 inclusive, concerning treatment and mortality rate after a six month period. To be included in the study, acute myocardial infarction had to fulfill particular inclusion criteria. A total of 1863 cases of acute myocardial infarction were included.
The mortality rate of patients with acute myocardial infarction treated with thrombolytic agents was strikingly lower and statistically very significantly different (p < 0.001) in comparison with the mortality rate of patients treated with heparin or coumarine derivatives.
The mortality rate dropped from 10.57% in the coumarine group and from 14.95% in the heparin group to 5.41% in the alteplase group, to 4.95% in the anistreplase group and 4.00% in the streptokinase subgroup.
The complications directly connected to the treatment did not seem to be different between the five groups, and they were also not more frequent by using thrombolytic agents.
In the last 20 years, better preventive measures (life habits, diet, medication) and trials to better control the risk factors have not influenced greatly the average amount of cholesterol in patients with an acute myocardial infarction. Also the percentage of patients with high blood pressure has hardly decreased over the last 20 years.
The mortality associated with acute myocardial infarction has decreased significantly with the use of thrombolytics. In most cases, thrombolytics are administered routinely and safely. In this way, they are the first choice therapy for myocardial infarction in smaller hospitals.
To obtain excellent coronary patency, thrombolytic agents with a long half-life and with PAI-1 resistance are required in the future.
The current measures and medical therapies seem to be insufficient to control the risk factors for coronary atherosclerosis.

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Short-term heparin therapy has been administered routinely after primary coronary stenting. However, heparin therapy results in a significantly higher incidence of bleeding and vascular complications. A new therapeutic regimen of ticlopidine and aspirin without further heparin after coronary stenting in patients without AMI has been shown to be safe and reduce the incidence of stent thrombosis. The aim of this study was to evaluate whether a new therapeutic regimen of aspirin and ticlopidine without heparin is safe and effective in patients with acute myocardial infarction (AMI) who have undergone primary coronary stenting and have Thrombolysis in Myocardial Infarction (TIMI) grade 3 flow in the infarct-related artery.
Between January 1997 and September 1999, one hundred and fifty two consecutive patients with AMI on Killip score 1 or 2 who underwent primary coronary stenting resulting in TIMI grade 3 flow were enrolled and divided into two groups: Group 1 (n = 95 patients) received aspirin, ticlopidine and further intravenous heparin infusion for 48 hours following primary coronary stenting; Group 2 (n = 57 patients) received only aspirin and ticlopidine without further heparin therapy following primary coronary stenting. No in-hospital major cardiac events were observed in either group. However, the combined incidence of bleeding and vascular complications (27.4% vs 12.3%, p = 0.029) and the need for blood transfusions (9.5% vs 0%, p = 0.013) were significantly higher in Group 1 patients. Furthermore, hospital stay was also longer in Group 1 patients (5.8 ± 2.4 vs 4.7 ± 1.7 days, p = 0.0003). At the 30-day follow-up, there were no differences (1.05% vs 0%, p = 0.63) in the combined incidence of vascular complications and the major cardiac events were similar (1.05% vs 1.75%, p = 0.71) between the groups.
The results suggest that further heparin therapy following primary coronary stenting increases the combined incidence of bleeding and vascular complications as well as the need for blood transfusions and prolongs the length of hospital stay without further benefit to those patients with coronary flow restored to TIMI 3 grade flow.

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Prolonged QT interval is suggested to indicate an increased risk of sudden cardiac death in certain clinical conditions such as diabetes mellitus. We investigated whether the individual QT interval is an indicator of an autonomic state. An ambulatory 24-hour ECG was recorded in 53 subjects from different clinical backgrounds. Power spectral components of heart rate variability (HRV) and the QT interval were regressively obtained at a heart rate of 60, 70, 80, 90, or 100 beats per minutes (bpm). Log values of the high-frequency component of HRV (HF: 0.15-0.50 Hz, a scale of cardiac parasympathetic tone) failed to show a relationship with the QT interval. In contrast, the QT interval at a heart rate of 90 bpm and 100 bpm showed a significant correlation with the log values of the low-frequency component (LF: 0.04-0.15 Hz) and the log[LF / HF], i.e., a putative scale of sympathetic tone (100 bpm: QT vs logLF: r = 0.414, p < 0.005, QT vs log[LF / HF]: r = 0.416, p < 0.002). Also, attenuated rate-dependent QT shortening was associated with greater logLF and log[LF / HF] values at a heart rate of 80, 90, or 100 bpm. These results suggest that the QT interval at a moderate heart rate (approximately 90-100 / min) and the degree of rate-dependent QT shortening are related to individual sympathetic tone.

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We evaluated left atrial systolic function using left atrial ejection force (LAEF) in 19 patients with sick sinus syndrome (SSS) and in 20 with paroxysmal atrial fibrillation (Paf) whose ages ranged from 48 to 80 years. We also evaluated 35 normal individuals for comparison. The LAEF was calculated as 1 / 3 × mitral valve area × (peak velocity of A wave)² using two-dimensional and pulsed-Doppler echocardiography according to Newton's law of motion and hydrodynamics. In normal individuals, LAEF positively correlated with age (r = 0.82, p < 0.01). Normal LAEF was calculated as 0.098 × age - 0.74 (kdynes) from the regression line. Because of this correlation, we used age-corrected LAEF (%LAEF) that was calculated as (measured LAEF / normal LAEF) × 100. The results showed that this value was 53 ± 26% in patients with SSS and 54 ± 26% in patients with Paf. Both were significantly lower than normal individuals (p < 0.001). Among SSS subtypes, %LAEF was lower in types II and III than in type I (51 ± 14%, 37 ± 19%, and 81 ± 35%, respectively). In conclusion, left atrial systolic function is depressed in patients with Paf and SSS, in particular, types II and III. These results suggest that the pathological abnormalities extend not only to the sinus node but also to the left atrial muscle in patients with SSS and Paf.

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Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a specific heart muscle disease of unknown etiology characterized by fatty and fibrofatty replacement of the right ventricular myocardium. It often manifests life-threatened ventricular arrhythmias. Previous studies have hypothesized that myocyte apoptosis contributes to the myocyte cell loss and fatty change in ARVC and may be induced by recurrent ventricular tachycardia (VT). We examined whether these progressive pathological changes result from apoptotic cell death in both autopsied and biopsied right ventricular myocardium from 35 patients with ARVC by using in situ terminal deoxynucleotidyl transferase assay (TUNEL) and agarose gel electrophoresis. We also studied the biopsied myocardium from 30 patients with idiopathic sustained VT whose origin was the outflow tract of the right ventricle. TUNEL-positive cells indicating DNA fragments were observed in some cardiomyocytes and fibroblasts in ARVC, but the numbers of TUNEL-positive myocytes were very low in idiopathic VT. DNA laddering was confirmed in two autopsied cases in ARVC, but not in a non-cardiac case who died. These results suggest that at least some cardiomyocytes and fibroblasts are subjected to apoptosis in ARVC, leading to the loss of myocardium with characteristic pathological changes and subsequently progressive cardiomyopathy. Furthermore, the apoptotic process may not result from myocardial ischemia due to repetitive VT.

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The aim of the present study was to characterize endothelium-dependent and -independent coronary functions in remodeling hearts after infarction. First, echocardiography showed that the left ventricular diastolic dimension and thickness of the non-ischemic region were increased by 25% and 20%, respectively, at 2 weeks after coronary ligation in the rabbit heart. In the second series of experiments, 2 weeks after coronary ligation or a sham operation, the heart was isolated and perfused with modified Krebs-Henseleit buffer at 75 mmHg, and effluent from the pulmonary artery was measured as total coronary flow (CF). Regional CF analysis by microspheres indicated that flow to the infarcted region as a percentage of total CF is negligibly small. There was no significant difference between CF responses to sodium nitroprusside (10^-9 - 10^-5 mole/l) in the sham-operated and remodeling hearts. However, the increase in CF after acetylcholine (ACh: 10^-8-10^-5 mole/l) injection was significantly reduced by approximately 50% in the remodeling hearts compared to that in the sham-operated hearts. Furthermore, the percent increase in CF by ACh (10^-5 mole/l) was inversely correlated with weight of the remodeling myocardium (r = -0.630, p < 0.05). These results suggest that endothelium-dependent vasodilatory function is impaired in the myocardium at the early stage of post-infarct remodeling and that this endothelial dysfunction is closely related to the degree of hypertrophy of the remodeling myocardium.

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A 56-year-old Japanese male with delayed cardiac tamponade which occurred 13 months after coronary artery bypass grafting (CABG) is presented. The patient was admitted to our hospital suffering from dypnea due to cardiac tamponade. Pericardiocentesis yielded a viscous bloody fluid. The patient recovered after continuous drainage followed by an intra-pericardial administration of minocycline hydrochloride. Sclerosant therapy is considered to be a treatment of choice for delayed cardiac tamponade following CABG.

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A 58-year-old Japanese man with variant angina developed acute myocardial infarction (AMI). Emergency coronary angiography demonstrated thrombotic occlusion in the proximal site of the left anterior descending artery. The occluded region appeared to be coincident with the area in which severe vasospasm had been provoked by intracoronary administration of acetylcholine 1.5 years before the onset of AMI. This case may give us a unique opportunity to consider the role of vasospasm in the etiology of AMI.

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In a patient with Wolff-Parkinson-White syndrome whose accessory pathway was primarily capable of bidirectional conduction, antegrade conduction over the accessory pathway was transiently inhibited after rapid atrial or ventricular pacing or after spontaneous termination of atrioventricular reentrant tachycardia. Pacing rate and duration of tachycardia were related to the duration of the suppression of preexcitation, while the coupling interval of the first sinus beat to the last driven or tachycardia beat was irrelevant to the phenomenon. Thus, overdrive suppression of conduction may be the most likely mechanism of this phenomenon.

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Mechanical complications of acute myocardial infarction (AMI) such as a ventricular septal defect (VSD) usually occur within the first week. In the thrombolytic era, the incidence of a VSD has not increased, but has been reported to occur earlier than previously described. We report an unusual case of an elderly Caucasian female with an acute anterior wall myocardial infarction treated with thrombolytic therapy. Her AMI was complicated by pulmonary edema secondary to a VSD and a left ventricular aneurysm five weeks later. Prompt diagnosis, immediate surgical closure of the VSD, and aneurysmectomy resulted in her complete recovery.

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A 69-year old Japanese woman with hypertension was admitted because of continuous back pain and recurrent hemoptysis. Radiographic findings showed an enhanced irregular mass, at the aortic arch fed by the tracheal artery, which implied both a penetrating aortic atherosclerotic ulcer and lung cancer. Diagnostic surgery revealed no evidence of cancer but did reveal a rupture of the intima at the distal part of the aortic arch. It is assumed that the transmural oozing occurred after development of the penetrating aortic ulcer, which formed an extra-aortic hematoma and caused surrounding inflammation, and led to tracheal artery feeding. The intramural hematoma might have weakened vascular wall tension from the aorta, and formed an oozing extra-aortic hematoma instead of an acute rupture.

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Stroke is an important complication for the surgical treatment of type A aortic dissection and it occurs immediately post operation. Many surgical techniques such as deep hypothermic circulatory arrest and retrograde cerebral perfusion have been reported to ameliorate this complication. We report here a male Taiwanese patient with type A aortic dissection involving the arch who underwent surgical repair. Amaurosis fugax appeared on the 4^th day post operation. Funduscopic findings demonstrated multi focal embolization and carotid sonography revealed normal carotid arteries. The symptoms and signs improved after anticoagulation therapy. This is a rare case of delayed onset of amaurosis fugax in a patient with type A aortic dissection post surgical repair. The thromboemboli might have originated from the internal surface of the sawing area.

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