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In a retrospective study, we tested the hypothesis that anticoagulant therapy with warfarin sodium (Coumadin) has a beneficial influence on the long-term prognosis in patients with primary pulmonary hypertension (PPH) and aminorex-induced plexogenic pulmonary hypertension. The study included a total of 173 patients from two European cities. One hundred four of these patients took the anorectic drug aminorex (Menocil), which was available in some European countries almost 30 years ago; 69 patients had pulmonary hypertension of unexplained etiology, ie, PPH. Fifty-six of the 104 aminorex-treated patients and 24 patients in the PPH group received warfarin after diagnosis was established. For analysis, patients were divided into four groups according to their history of aminorex intake and anticoagulant therapy. Survival time, changes in hemodynamics (pulmonary arterial pressure), and improvement in quality of life (scored by the New York Heart Association [NYHA] classification) were compared and analyzed. We found that aminorex-treated patients had a better long-term prognosis than those with PPH (7.5 vs 3.9 years; p < or = 0.001). The best mean survival time of 8.3 years was found in anticoagulated aminorex-treated patients, compared to 6.1 years in nonanticoagulated aminorex-treated patients. Moreover, aminorex-treated patients who received anticoagulant therapy soon after the onset of symptoms showed significantly better prognosis (10.9 years) than those who commenced treatment 2 years thereafter (5.9 years) (p < or = 0.05). In patients with PPH, systolic pulmonary pressure was shown to influence survival time significantly (p < or = 0.0005); however, this correlation was not found in aminorex-treated patients. An improvement of symptoms like dyspnea on exertion was seen in 44.8% of the anticoagulated aminorex-treated patients, while deterioration was evident in 72.2% of the nonanticoagulated aminorex-treated patients. In conclusion, our study has shown that anticoagulant therapy had a positive influence on long-term survival and a significant improvement in quality of life in patients with PPH, in particular in patients with a history of anorectic drug intake.

The purpose of this study was to examine the influence of treatment on long-term prognosis of patients with aminorex-induced plexogenic pulmonary hypertension. The study included 104 patients (13 males, 91 females) with an aminorex (menocil) intake between 1966 and 1968. All patients were treated with digitalis and diuretics, 52% received an anticoagulant medication with warfarin after pulmonary hypertension was diagnosed. During follow-up, a second right-heart catheterization was performed in 37 patients with a mean interval of 5 years. The longest mean survival time, 8.3 years, was found in patients treated with anticoagulant medication, compared to the 6.1 years found in the non-anticoagulated aminorex patients. Also, in the 5- and 10-years survival rate, patients with an anticoagulant therapy have shown better results (62.9 vs. 38% and 39 vs. 20%, respectively). Patients who received anticoagulant therapy soon after the onset of symptoms showed a better mean survival (10.9 years) than those who commenced treatment more than 1 year thereafter (mean survival 5.9 years). In 57% of the patients who had a second right-heart catheterization a decrease of pulmonary pressures could be diagnosed. Two-thirds of these patients with pulmonary pressure decrease were under anticoagulant therapy. An improvement in the NYHA-classification was seen in 44.8% of the patients treated with warfarin, in comparison to 22.2% of those who did not receive anticoagulant therapy. Although this study is retrospective, it shows a positive influence of anticoagulant therapy on survival in patients with a history of anorectic drug intake.

Three young female patients with heart problems and positive serologic tests or characteristic histologic lesions for Chagas' disease (American trypanosomiasis) are reported, one of them having presented with acute anterior myocardial infarction with only minor coronary lesions. The most prominent features of the disease are discussed with emphasis on late cardiac complications. Chagas' cardiomyopathy is the leading cause of sudden death in Latin America, where an estimated 10 to 12 million people are infected in endemic areas from southern Mexico to southern Argentina. It has also been termed "emboligenic cardiomyopathy" since arterial embolism is a very frequent complication. Embolic obstruction of a coronary artery may therefore well be the most probable cause of myocardial infarction in young people with Chagas' disease, although other mechanisms cannot be excluded.

Eight patients with HOCM from the same family are presented. The clinical findings and the diagnostic and therapeutic procedures are discussed. Chest pain, palpitations and effort dyspnea were the main clinical symptoms. A characteristic systolic ejection murmur of late onset was present in all the cases. In 6 patients there were electrocardiographic signs of left ventricular hypertrophy and only 4 patients exhibited abnormal septal depolarization. Echocardiography revealed an enhanced diastolic interventricular septal to left ventricular posterior wall ratio (above 1.3), diminished left ventricular septum movement, systolic anterior motion of the mitral valve and mid systolic closure of the aortic valve. Cardiac catheterization showed a left ventricular out-flow gradient which was increased by isoproterenol infusion. In 5 patients the left ventricular angiogram disclosed systolic obliteration of the left ventricle and in 4 cases mitral regurgitation. In the therapy of HOCM, calcium antagonists are now widely used and seem to have replaced betablocking agents.

A local cold exposure test of the nailfold capillaries produces a typical flow stop reaction in 88% of patients with Raynaud's phenomenon. We applied this test to 12 patients with variant angina and compared the results with the findings in 2 control groups of 12 patients each, matched for age and sex: One group with chronic stable angina and one without heart disease. We found a flow stop with cold exposure in 9/12 patients with variant angina (mean duration 24 s), in 6/12 patients with chronic angina (mean 11 s), and in 1/12 normal controls without heart disease (mean 1 s). The frequency and duration of the flow stop was significantly higher in patients with variant angina (p = 0.002) and in patients with chronic stable angina (p = 0.02) than in normal controls. Patients with variant angina also tended to have an increased frequency and longer duration of the flow stop than those with chronic stable angina (p = 0.09). Administration of sorbidilate preparations and nifedipine resulted in a decrease of the mean flow stop duration from 23.5 to 10.8 s in patients with variant angina (p = 0.03). The strong association of a vasoconstrictive reaction in finger microcirculation and coronaries in patients with variant angina suggests a vasospastic tendency with manifestation in different vascular regions.

A computer-assisted model for quantitative analysis of left ventricular segmental wall motion is presented. In contrast to standard rectangular and radial chord methods, no coordinate and reference system is used. Normal wall motion of 5 ventricular segments in the RAO projection was evaluated in 20 patients with normal ventriculograms. Segmental wall motion abnormalities after myocardial infarction were then analyzed by the computer-assisted method in 60 patients and the results compared with the visual assessment of an experienced cardiologist as standard reference. 96% of all segments with normal motion, 95% of all hypokinetic segments and 100% of all dyskinetic segments were correctly identified by computer analysis. Akinesia, however, was detected only in 25% of all cases and misinterpreted chiefly as hypokinesia. Further refinement of the software should improve detection of akinesia and classification of hypokinesia.

The sudden and transient loss of consciousness and muscular tone from which the patient usually recovers spontaneously, i.e. syncope, is a frequent symptom. Diseases of the heart with and without rhythm disturbances together with disorders of the reflex, in particular the orthostatic regulation of the circulation, are among the main causes of syncopal events. The pathophysiological mechanisms of cardiovascular syncopes are manifold, and more than one factor can contribute to a single mechanism. Their aetiological assignment may be straightforward, but sometimes requires laborious and expensive investigational procedures. The treatment of a syncopal attack ranges from simple manipulations to true reanimation, its long-term prevention from antiarrhythmic drugs to major heart surgery, and its prognosis from the bagatelle to sudden death.

Ethyl ether dissolved in saline has been used as an indicator for measuring cardiac output in patients with various congenital and acquired valvular heart diseases without shunts. The solution was infused at a constant rate into the superior vena cava. By means of a simultaneous rebreathing maneuver it was possible to determine the ether concentration of the mixed venous blood and hence the dilution factor. Comparative measurements with the direct Fick method revealed a satisfactory accuracy of the ether dilution method (r = 0.94), which does not require sampling and analysis of mixed venous and arterial blood.

Serum apoprotein and lipid concentrations were measured in 63 patients undergoing coronary angiography. Thirty-eight patients had 50% or higher grade stenoses, 25 had chest pain, but no significant stenoses. Among the patients with higher grade stenoses 71% had hyperlipoproteinemias as opposed to 12% in patients without stenoses. As compared to suitable normal controls, patients with angiographically documented coronary heart disease showed significant changes in all lipid and apoprotein concentrations under study. However, differences between the two patients groups were also noted. Among these, apo A-I, A-II and B, total cholesterol and LDL cholesterol were statistically significant. These results indicate that apoprotein A and B levels, total cholesterol and LDL cholesterol are good discriminators of the severity of coronary heart disease, while HDL cholesterol is a more suitable parameter for epidemiological studies.

The introduction of selective coronary arteriography and aorto-to-coronary saphenous vein bypass surgery (a.-c bypass) has fundamentally altered our understanding of ischemic heart disease (IHD). The indications for the effective diagnostic procedure and the results of the new and increasingly important surgical technique are summarized. Selective coronary arteriography should be performed (a) in patients with known IHD in order to furnish the anatomical and functional information necessary to assess the indication for surgery, i.e. in patients below 60 years with intractable stable or unstable (impending infarction) angina. It is rarely indicated in patients with an old myocardial infarction who are free from symptoms. It is debatable in patients during the acute stage of infarction; (b) in patients with questionable IHD, with the aim of ruling out or confirming the condition, i.e. mainly in patients with atypical chest pain or with equivocal ecg findings. The risks of the procedure, if carried out by experienced personnel, are small. Selective arteriography will always be supplemented by a selective left ventricular angiography yielding important information concerning the functional behaviour of the myocardium. In judging the therapeutic value of a.-c. bypass surgery it should be noted that postoperatively 60 to 70 percent of the patients present without symptoms and 80 to 95 percent feel markedly better, and that physical performance is enhanced in about the same proportions. An improvement in left ventricular function under exercise conditions seems to be rare. Hospital mortality of a.-c. bypass operation is small and below 5 percent if patients with stable angina and without myocardial failure, previous infarctions or mitral regurgitation are considered. In the presence of an ischemic cardiomyopathy, on the other hand, the mere surgical risk soon reaches prohibitive limits. The incidence of early complicating myocardial infarctions ranges around 10 percent. Bypass occlusion occurs in some 5 to 15 percent during the early postoperative phase, while in the following months and years the patency rate diminishes but little. If the survival rates of operated and non-operated patients with IHD are compared it becomes evident that a prolongation of life is possible whenever surgery aims at a correction of two- and three-vessel disease (including the prognostically unfavourable isolated stenosis of the left anterior descending branch and stenosis of left main artery) whereas the natural course of isolated lesions of the right coronary artery and the left circumflex branch seems to balance the effect of corresponding surgical interventions. It should be borne in mind, however, that the follow-up periods on which these statements are based do not exceed 3-4 years.

A study was designed to examine ventricular arrhythmias in the acute phase of experimental myocardial infarction in the pig and to evaluate possible antiarrhythmogenic influence of the beta-adrenergic blocking drug pindolol (Visken) and the calcium antagonist Ro 11-1781. Ventricular fibrillation (VF) occurred in 17 of 18 animals, in 4 almost immediately after coronary occlusion and in 12 with a delay of about 17 min. VF was almost always induced by episodes of ventricular tachycardia (VT) which were started by single ventricular premature beats (VPBs). VPBs occurred in 3 phases, whereas VT and VF coincided only with phase 1 and phase 3. The prematurity index QR/QT of single VPBs decreased significantly with time after coronary occlusion. The beta-adrenergic blocking drug pindolol and the calcium antagonist Ro 11-1781 did not prevent VT or VF.

A small fraction of a commercially available kit for the preparation of human serum albumin (HSA)-microspheres is labeled with 111In or 99mTc. The regional coronary blood flow is determined after selective injection of these labeled microspheres at rest and during rapid atrial pacing using a double-isotope coronary scintigraphy with a gamma camera.