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The study group included 30 middle-aged patients (mean = 47.0 +/- 0.6 years) with chronic heart failure (NYHA class III and IV) in the course of primary dilated cardiomyopathy and ischemic heart disease. Enalapril in a dose of 5-10 mg/day was added to previous therapy with digitalis and diuretics. The patients were submitted for noninvasive cardiac and biochemical studies initially and at 3 months. Twenty-four patients completed the planned therapy. In 5 patients the drug had been withdrawn due to hypotension, and one patient died on the fourteenth day of observation because of heart failure worsening. After enalapril therapy 18 patients improved in NYHA functional classes. All patients showed left ventricular improvement based upon left ventricular systolic time intervals, 18 patients showed reduced peripheral vascular resistance, and in 9 patients echocardiography revealed a significant improvement of EF, CI and mVCF. Renal function also improved based upon the decrease in urea and uric acid.

The study aimed at assessing a relationship between pain and panic in the echocardiographically confirmed mitral valve prolapse syndrome. Thirty three patients, 23 women and 10 men, were included. Mean age was 32 years. Standard Pain Perception Questionnaire by Melzack and Ostrowski's Well Being Questionnaire were used. During examination all patients were free from pain. Therefore, delayed pain effect was assessed. Present pain was evaluated with different scale. Significant relationship between pain and panic was shown in the mitral valve prolapse syndrome. In retrospective analysis pain was responsible for 16% of panic disorders (n = 0.396; p < .02). An effect of the actual pain is less pronounced and explain 14% of panic disorders (n = 0.372; p < .02), as the actual pain was less intense. There was also contrary relationship, but weaker. Panic exerts an effect on pain intensity in 11% (n = 0.330; p < .05). In the system pain-panic the former is prevailing in this syndrome. The obtained results confirm the value of psychotherapy modifying panic disorders.

The aim of this study was to evaluate a possible relation between the autonomic tone determined by daily urine catecholamine excretion and the incidence of ventricular arrhythmias (VA) in patients with mitral valve prolapse (MVP). The study included 53 patients (31 women and 22 men) aged 19-52 years (mean age 32.7). The diagnosis of MVP was based on medical history, physical examination, and echocardiography. Cardiac arrhythmias were detected by Holter monitoring and classified according to Lown grades. Daily heart rate and duration of corrected QT interval using Basett's formula were also analyzed. Daily urine adrenaline and noradrenaline levels were determined fluorometrically by Von Euler and Lishajko's method. The patients with Lown's grade III-V VA were evaluated with particular consideration. Student's t-test was used for statistical analysis. On Holter monitoring 26 patients showed VA, including 6 with grade I, 11 with grade II, 2 with grade III, 4 with grade IV, and 3 with grade V according to Lown's classification. The remaining 27 patients were free of cardiac arrhythmias. Mean daily heart rate ranged from 54-93 beats/min (73 +/- 8.44, mean +/- SD) and corrected QT from 336-494 ms (411 +/- 37.17). Daily adrenaline and noradrenaline excretion for the whole group of patients were 0.01-16.2 micrograms (2.1 +/- 2.38) and 1.6-31.0 micrograms (13.1 +/- 7.27), respectively, which was within normal range. However, the patients with serious ventricular arrhythmias showed significantly higher daily adrenaline excretion. Individual analysis of two-thirds of patients with ventricular arrhythmias grade III-V showed daily urine noradrenaline levels exceeding mean values for the whole group.(ABSTRACT TRUNCATED AT 250 WORDS)

A double-blind study was performed in 32 patients with stable angina pectoris to assess the effects of slow-release isosorbide dinitrate (ISDN) (a single dose of 120 mg/day) on the frequency and duration of painless and painful ischemic episodes, and on electrocardiographic changes and exercise tolerance. Forty-eight-hour electrocardiographic monitoring and treadmill exercise tests were performed before, and at 20 and 21 days of therapy. Holter monitoring showed a significant decrease in the frequency of painful and silent episodes (p less than 0.001), and in the duration of painful (1,623 +/- 664 seconds vs 323 +/- 161 seconds; p less than 0.001) and silent episodes (2,818 +/- 1,496 seconds vs 223 +/- 102 seconds; p less than 0.001). The magnitude of painful and silent ST-segment depression was significantly reduced (2.7 +/- 0.9 mm to 0.7 +/- 0.7 mm and 2.0 +/- 1.1 mm to 0.7 +/- 0.5 mm, respectively; p less than 0.001). Time of exercise testing to the onset of ST-segment depression (442 +/- 137 seconds vs 858 +/- 110 seconds; p less than 0.001) or anginal pain was doubled (461 +/- 128 seconds vs 830 +/- 130 seconds; p less than 0.001). The work load increased from 6 to 10 METs (p less than 0.001). ISDN in a single dose of 120 mg/day is a valuable drug for stable angina pectoris, decreasing the frequency of silent and painful ischemic episodes and the magnitude of ST-segment depressions, and increasing exercise tolerance. It particularly shortened the duration of silent episodes. For patients' compliance, a once-daily dose of ISDN could be advantageous.

Unlabelled: A decrease in the myocardial extraction or excretion of lactates indicates its hypoxia. The authors analyzed changes in the extraction of lactates, non-esterified fatty acids (NEFA) and their fractions: C 14:0, C 16:0, C 16:1, C 18:1, C 18:2 in a group of 15 patients with dilated cardiomyopathy (DC) and in 10 controls at rest and after the cold pressor test (CPT). At rest, 5 patients with DC produced lactates or extracted less than 10%. During CPT, production of lactates was observed in another four patients (mean values: 17.9 +/- 32.6% vs 24.5 +/- 5.2%, ns). NEFA extraction was found in the DC group: 18.4 +/- 20.6% vs. 13.9 +/- 33.3% /p < 0.05/). The acids involved were C 14:0, C 16:0, C 16:1 and C 18:0. In the controls, NEFA extraction did not change significantly: 12.1 +/- 8.6% vs 29.7 +/- 33.2%., Conclusions: 1. In part of patients with DC, production of lactates was found. The degree of lactate excretion increased due to CPT; 2. In DC, adrenergic stimulus (CPT) impairs the myocardial utilization of NEFA. This applied mainly to myristic acids, palmitic acid, palmitooleic acid and stearic acid; 3. This phenomenon probably is a result of profound functional and morphological damage to the mitochondrial system in DC.

The purpose of the study was to analyse relationships between the presence and magnitude of a regurgitant wave from the left ventricle to the left atrium and the state of the pulmonary circulation in patients with primary dilated cardiomyopathy. The study population consisted of 97 patients divided into three subgroups I--41 patients without the regurgitant wave, II--31 patients with the first-degree regurgitant wave, III--25 patients with the second-degree regurgitant wave. Diagnosis was based upon non invasive studies, cardiac catheterization and left ventriculography. Average values of the left ventricular systolic and end-diastolic pressures were similar in all subgroups, whereas the cardiac index was the lowest in the subgroup of patients with a large regurgitant wave to the left atrium. There were no differences in mean values of the pulmonary artery pressures, total pulmonary resistance and pulmonary vascular resistance between the patients without the regurgitant wave (subgroup II). In contrast the patients with a large regurgitant wave (subgroup III) showed statistically significantly higher pulmonary artery pressures, higher total pulmonary resistance and pulmonary vascular resistance. In 64% of the patients of this subgroup the left atrium was said to be large. The results of the present study indicate that even not a large regurgitant wave (second-degree) from the left ventricle to the left atrium leads to secondary pulmonary hypertension in patients with primary dilated cardiomyopathy.

An effect of isosorbide dinitrate on blood pressure values in the pulmonary circulation and the right heart has been investigated in 25 patients with a history of the first transmural myocardial infarction. Group I including 12 patients has been given 5 mg isosorbide nitrate in a 60-minute intravenous infusion while group II of 13 patients has been given 10 mg of the drug in the same way. Both groups have been matched in clinical data and blood pressure value in the pulmonary circulation which has been normal. Pulmonary blood pressure has been measured with Swan-Ganz catheter prior to the administration of drug, and 15, 30, 45 and 60 minutes following an infusion. Isosorbide dinitrate in a dose of 5 mg did not decrease blood pressure in the pulmonary circulation statistically significantly. The differences in blood pressure falls did exceed 9%. Filling pressure in the right ventricle did not change either while systolic blood pressure decrease by 16.6%. A double dose of isosorbide dinitrate reduced blood pressure in the pulmonary artery by about 1/3 of the baseline value, and blood pressure in the right ventricle (mean right atrial pressure) by 57.2%. Both systolic and diastolic arterial pressures were reduced. Isosorbide dinitrate reduced blood pressure in the pulmonary circulation in patients who underwent myocardial infarction, and hypotensive effect has been dose-related. A reduction in the right ventricular filling pressure has been a one of important mechanisms decreasing pulmonary pressures.

The aim of the study was to investigate whether oxygen causes a further decrease in pulmonary artery pressure after administration of calcium channel blocker-verapamil-or angiotensin converting enzyme inhibitor-captopril-in the secondary pulmonary hypertension. We studied 37 patients with the secondary pulmonary hypertension (mean pulmonary artery systolic pressure = 56.1 mm Hg) due to mitral stenosis. After having completed hemodynamic diagnostic procedures, basal oxygen test was performed and pulmonary artery pressure was recorded at 10 min of oxygen breathing. Then, 10 mg of verapamil was injected into the pulmonary artery of 16 patients and 21 patients received 75 mg of oral captopril. At the peak of vasodilation, 30 min after verapamil and 90 min after captopril administration, pulmonary artery pressure was recorded and oxygen test was repeated. Baseline oxygen test produced a statistically significant decrease in pulmonary artery pressure. Verapamil and captopril also lowered pulmonary artery systolic and diastolic pressures. The second oxygen test did not cause a further decrease in the pulmonary artery pressure; mean pulmonary artery systolic pressure was 52.3 +/- 23.7 mm Hg, pulmonary artery diastolic pressure 22.7 +/- 10.6 mm Hg before and 49.1 +/- 23.8 mm Hg and 23.0 +/- 13.5 mm Hg, respectively after the test in verapamil group, and 47.0 +/- 15.5 mm Hg and 21.7 +/- 8.4 mm Hg before and 46.6 +/- 15.4 mm Hg, respectively in captopril subset. The results may support the thesis that vasodilating effect depends rather on the degree of pulmonary vascular changes than on the vasodilatory mechanism of particular drugs.

Selected parameters of the pulmonary circulation and right ventricular performance were studied in 30 patients with primary arterial hypertension. Four patients belonged to the WHO class I, four to class I/II, 18 to class II and the remaining four to class III. Patients were eligible, if they were in sinus rhythm, without symptoms of left ventricular failure and diseases that night influence pulmonary pressures, and if drugs affecting cardiac performance could be withdrawn safely for 3 days. Ten healthy subjects served as control group. The mean pulmonary capillary wedge pressure and mean pulmonary artery pressure were similar in both groups. In contrast, the systolic pulmonary arterial pressure exceeded 30 mm Hg in 6 patients. Mean pulmonary vascular resistance was higher in examined patients than in the control group. Right ventricular end-diastolic pressure was above 5 mm Hg in as much as 50% of patients. Mean systolic ejection rate showed a tendency to decrease. The results indicate that part of patients with primary arterial hypertension exhibits disorders in the pulmonary circulation and right ventricular performance.

Left ventricular hypertrophy in arterial hypertension occurs in over 50% of patients. The detection of such high incidence has been facilitated by the introduction of echocardiography into diagnostic studies. Both earlier electrocardiographic findings and later echocardiographic results show that cardiac hypertrophy leads to an increased mortality and predisposes to cardiac arrhythmias, ischemic heart disease including myocardial infarction and heart failure. The development of hypertrophy is mediated by hemodynamic factors such as elevated blood pressure due to increased peripheral vascular resistance, ejection fraction, increased cardiac output, blood viscosity, as well as by non-hemodynamic factors. Of the latter ones the contribution of a genetic factor is discussed, whereas the role of para- and autocrine cardiac function manifested by local production and action of catecholamines as well as the renin-angiotensin system has been proved. Blockade of these systems makes possible prevention of the development of cardiac hypertrophy or its regression. Such results have been obtained both in experimental studies and in humans with hypertension treated with selected drugs. Regression of hypertrophy is accompanied by an improvement in systolic and especially diastolic cardiac function, the impairment of which is usually diagnosed prior to the detection of hypertrophy. The improvement in cardiac function and possibility of preventing consequences of hypertrophy help us to evaluate the efficacy of hypotensive drugs and their preferential use in this regard. There are also changes in recently recommended models of pharmacological treatment in arterial hypertension.

The effects of nifedipine in a single dose of 10 mg on the pulmonary circulation and the selected right and left ventricular function indices were studied in a group of 10 patients with secondary pulmonary hypertension (mean systolic pressure 55.2 mm Hg). In 8 patients hemodynamic studies were repeated after seven days treatment (3 x 10 mg). Acute treatment with nifedipine resulted in a reduction in mean systolic arterial pressure by 21.8%, diastolic by 12.2% and systemic resistance by 25.5%, and in an increase in cardiac index by 14.3%. After 7 days a similar pattern of changes was observed, however with less intensity: systolic pressure was reduced by 10.3% diastolic by 5.5%, and systemic resistance by 17.1%. Pulmonary artery wedge pressure did not change after a single dose, and mean pulmonary artery pressures showed a tendency toward lower levels: systolic by 8.9% and diastolic by 8.6%, whereas total pulmonary resistance decreased markedly (by 22.7%), as well as pulmonary vascular resistance. Right ventricular filling pressure was reduced. After chronic treatment we found a further slight fall in the pulmonary arterial pressure. Although per cent changes were similar to those in the arterial pressure, alterations in the mean values were not statistically significant. The total pulmonary resistance remained reduced. While analysing the changes in the pulmonary circulation and right ventricular indices it should be noted that they were less intense and less homogeneous than the left ventricular function parameters. Some of the patients showed certain similarities in the direction and intensity of changes in the hemodynamic indices of the pulmonary circulation in the acute and chronic experiment.

Etiology of constrictive pericarditis is diversified. In recent years the role of viral and iatrogenic factors (X-ray therapy, cardiac surgery) has increased. Clinical manifestations, including subjective complaints, resemble those in congestive heart failure although the mechanism of hemodynamic disorders is different--namely impairment of ventricular filling and diastolic performance. One encounters major difficulties while differentiating constrictive pericarditis from restrictive cardiomyopathy. In some patients conservative treatment is effective, in a majority of them surgical operation, pericardiectomy is the treatment of choice.

In 35 patients with ischemic heart disease we evaluated the incidence of ventricular late potentials and left ventricular function. The patients were divided into two groups: group A consisting of 15 patients (14 men, 1 woman) aged from 40 to 71 years (mean age 56) with previously documented ventricular tachycardia or fibrillation, and into group B comprising 20 subject (16 men, 4 women) aged from 35 to 62 years (mean age 50) with ischemic heart disease without the above-mentioned arrhythmias. Time from the development of ventricular tachycardia or fibrillation was 3 weeks to 4 years. The incidence of arterial hypertension and previous myocardial infarction was similar in both groups. Body surface late potentials were recorded by signal averaging technique according to Simson using Frank's orthogonal XYZ lead system. In addition, in all the patients 24-hour ECG monitoring was performed to reveal any ventricular rhythm disturbances and echocardiography was used to evaluate left ventricular function. The presence of the ventricular late potentials meeting at least two of the Simson's--Dene's criteria was found in 13 (87%) patients in group A and in 2 (10%) patients from group B. In the patients after ventricular tachycardia or fibrillation the mean values of th total QRS duration (QRS-D) and the low amplitude signal duration (LAS40) were higher whereas the root mean square voltage of the last 40 ms of th vector magnitude QRS (RMS) was lower (154 ms, 56 ms, 15 muV, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

The pericardium plays an important role in the normal cardiac work. Its major functions include: maintenance of adequate cardiac position, separation from the surrounding tissues of the mediastinum, protection against ventricular dilatation, maintenance of low transmural pressure, facilitation of ventricular interdependence and atrial filling. Congenital absence of the pericardium should be differentiated first of all from atrial septal defect ostium secundum type, idiopathic dilatation of the pulmonary artery and tumours of the left mediastinum.

To estimate frequency of the posterior mitral valve leaflet prolapse in routinely performed left ventriculography, 1000 consecutive ventriculograms of the right anterior oblique projection were analyzed. A group of patients consisted of 511 women and 489 men at mean age 46,5 years. Clinical diagnosis of heart lesions, myocardial disease, pulmonary hypertension or arrhythmias were indications for hemodynamic studies. In the investigated group of patients, there were no patients with clinical diagnosis of the coronary artery disease. Prolapse of the posterior mitral valve leaflet was diagnosed in 59 patients. Idiopathic mitral valve prolapse was diagnosed in 10 patients. Prolapse of the posterior mitral valve leaflet was most frequent in atrial septal defect (16.6%), myocardial lesion (12.5%), and after mitral commissurotomy (8.9%). Posterior mitral valve leaflet prolapse is not a frequent anomaly in routinely performed left ventriculography. Relatively often occurrence of the mitral valve prolapse in atrial septal defect and only occasional in the aortic lesions and dilated cardiomyopathy seems to point out at a role of the left ventricle size in pathogenesis of this syndrome.

Radionuclide angiography was performed during upright exercise to compare left ventricular function in nine regular runners to nine age-matched, healthy controls. Heart rate, blood pressure, left ventricular ejection fraction (LVEF), end diastolic volume index (EDVI), end systolic volume index (ESVI), and stroke volume index (SVI) were measured at rest and at 40%, 60%, 80%, and 100% of maximum work capacity (mean maximal workload [KPM +/- SD] was 1,773 +/- 157 in runners and 1,260 +/- 324 in controls). The resting data of runners and controls were similar. There were no significant differences in heart rate, systolic blood pressure, and LVEF between runners and controls during exercise. SVI and EDVI were higher in runners during exercise (P less than 0.05). ESVI was lower in controls at a 60% level of exercise (P less than 0.05). The data indicate that an early and sustained increase in the diastolic volume of the left ventricle is important for enhanced cardiac performance of regular runners during exercise.

Certain indices of pulmonary haemodynamics were determined at rest in 39 patients with constrictive pericarditis. The most frequent anomaly was raised value of total pulmonary resistance (in 82% of cases) and, in a lower percent, raised pulmonary vascular resistance. The systolic pressure in the pulmonary artery was raised in 30.8% of the patients, reaching values regarded as low or medium degree hypertension. In only 2 cases the systolic pressure in the pulmonary artery was 100 mm Hg or more. The systolic pressure in the pulmonary artery showed a slight positive correlation with the end-diastolic pressure in the left ventricle, and the subgroup with pulmonary hypertension had higher average values of the end-diastolic pressure in the left ventricle than patients with normal pressure in the pulmonary circulation (means = 21.0 +/- 5.7 vs 15.2 +/- 6.5 mm Hg). These results show a significant role of increased filling pressure of the left ventricle in the mechanism of pulmonary hypertension in patients with constrictive pericarditis.

The acute hypotensive effect of nifedipine was evaluated, and the possibility of its long-term use in hypertensives over 60 years of age was studied. Sublingual nifedipine in a dose of 20 mg was given to 28 patients, mean age 73.1 yrs, and blood pressure, heart rate, and plasma drug concentration were monitored at 15 min, and every 30 min thereafter for 3 hrs. Systolic and diastolic blood pressure decreased at 15 min by 22.1 and 7.0 mmHg, respectively, reaching a maximal decrease two hours after drug administration. The decrease in blood pressure level did not correlate with nifedipine plasma concentration, but only with the initial systolic blood pressure. Long-term treatment with nifedipine was initiated in 60 patients, with 45 patients completing the study. Mean age was 66.2 years. An initial dose of 30 mg daily had to be increased to 60-80 mg in one-third of the patients. Monotherapy was not satisfactory in some patients. Blood pressure gradually decreased from 173/99 to 148/85 mmHg at three months, and to 141/84 mmHg at six months. Drug tolerance was fairly good. Nifedipine was withdrawn due to a considerable increase in heart rate in three patients and skin allergy in one. The most frequent adverse symptoms were: rash, headache, and leg oedema. Laboratory tests revealed no changes in urea and creatinine, and an increase in fasting glycaemia. Lipid parameters did not change significantly. These data proved that a single dose of 20 mg of nifedipine produced therapeutic plasma concentration of the drug and good hypotensive effect, positively correlating with initial systolic blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Selected indices of left and right ventricular function and pulmonary circulation have been compared in two groups of patients with constrictive pericarditis: i.e. in 10 patients classified as NYHA functional class II and 13 patients as NYHA class III. The patients with NYHA class III showed higher average values of left ventricular end-diastolic pressure (mean + 19.4 vs 11.4 mm Hg) and right ventricular end-diastolic pressure (mean + 17.3 vs 9.5 mm Hg) as well as pulmonary systolic (mean + 39.5 vs 24.5 mm Hg) and diastolic pressure (mean + 20.6 vs 9.9 mm Hg). Mean total pulmonary resistance and left and right ventricular stiffness indices were slightly higher whereas cardiac index was slightly lower. Complaints of patients with constrictive pericarditis, fatigability and dyspnea are to a large extent determined by the level of end-diastolic pressure in both ventricles and pulmonary hypertension that is by similar direct mechanism as in congestive heart failure.

In a group of 37 patients (30 men and 7 women aged from 36 to 67 years, men age 50.3) after a first acute myocardial infarction the frequency was analysed of the episodes of silent myocardial ischaemia with ST depression, and its correlation with arrhythmia was studied during outpatient ECG monitoring and exercise test on cycle ergometer. Outpatient ECG monitoring during 24 hours was done with a recorder Oxford Medilog MR-14 AM System 8-12 weeks after the onset of infarction. In the same patients the exercise test on cycle ergometer (KF-12 Medicor) was done by graded exercise method with workload increasing by 25 Watt every 3 minutes. The test was terminated after achieving 85% maximal heart rate or appearance of limiting signs. Each episode of ST depression by 1.0 mm or more lasting over 1 minute with horizontal or sloping ST depression 80 msec from point J was regarded in both cases as ischaemic. During outpatient ECG monitoring it was observed that 30 out of 37 (81.1%) had 138 episodes of ST depression, including 45 (32.6%) associated with pain and 93 (67.9%) painless (p less than 0.02). The mean maximal ST depression during painful and painless episodes was respectively 3.4 +/- 1.3 mm and 2.9 +/- 1.1 mm (p less than 0.03). Out of 30 patients 7 (23.3%) had 54 episodes of various arrhythmias, with bursts of ventricular ectopic beats, in one patient supraventricular tachycardia and in another one grade II atrioventricular block developed. These patients had also isolated ventricular ectopic beats. In 6 patients (20.0%) arrhythmia was temporarily associated with signs of ischaemia with ST depression.(ABSTRACT TRUNCATED AT 250 WORDS)

The study aimed at evaluating a possible relationship between the adrenergic system tone determined with the excretion of catecholamines with the urine and an incidence of the ventricular arrhythmias in patients with the mitral valve prolapse. The study included 20 patients (13 women and 7 men aged between 20 and 50 years; mean = 31.6 years) with the mitral valve prolapse syndrome diagnosed with the aid of the patients' history, physical examinations and echocardiography. Echocardiograms have shown anterior mitral leaflet prolapse in 7 patients, posterior mitral leaflet prolapse in 8 patients, and both mitral leaflets prolapse in the remaining 5 patients. Daily excretion of adrenaline and noradrenaline was measured with Van Euler and Lishajko's fluorimetric technique. Cardiac arrhythmias were determined with a 24-hour ECG monitoring and classified according to Lown. Premature ventricular contractions of class I were seen in 1 patient, of class II in 5, class III in 1, class IV in 2, and class V in 3 patients. Holter monitoring technique did not show the arrhythmias in 8 patients. Daily adrenaline and noradrenaline excretion with the urine was within the normal values (3.2-30.8 ug and 0.2-16.2 ug, respectively) in all examined patients. Daily urine noradrenaline was higher in patients with serious ventricular arrhythmias (Lown's class V) than mean values in the whole examined group.

An analysis of cardiac arrhythmias in relation to left ventricular morphology and function was performed in 68 hypertensive patients 60 to 83 years of age. The study comprised Holter monitoring and echocardiography. Our results suggest that in elderly patients with primary arterial hypertension a correlation exists between left ventricular mass and the incidence of ventricular arrhythmias but not between left ventricular mass and supraventricular arrhythmias.

The paper presents an adverse effect of Lorcainide on the electrocardiographic pattern and left ventricular function in a patient with recurrent ventricular tachycardia in the course of arterial hypertension and ischemic heart disease. Based upon this case report a relatively new and not well known phenomenon of drug arrhythmogenesis is presented.

The purpose of the study was to assess effects various doses of isosorbide dinitrate (ISDN) on left and right ventricular systolic time intervals in patients after myocardial infarction. The study population consisted of 25 patients who were eight weeks after their first transmural myocardial infarction. Twelve patients were given 5 mg of ISDN by an intravenous infusion for 60 min, and remaining 13 patients were given 10 mg of ISDN in a similar manner. Subgroups did not differ with respect to their initial arterial blood pressure (mean = 133.3) 82.9 vs 134.3 (87.1 mm Hg) and systolic pulmonary arterial pressure (mean = 27.2 vs 28.8 mm Hg). The infarct localization was also similar. Left ventricular systolic time intervals were calculated noninvasively, whereas right ventricular systolic time intervals were measured from simultaneous electrocardiographic, phonocardiographic and pulmonary arterial pressure tracings. Both left and right ventricular systolic time intervals were determined before and at 15 and 60 min after the drug administration. Student's t-test for unpaired and paired variables was used to test for statistical significance. Changes in the parameters studied at 60 min of the ISDN infusion were greater than at 15 min, and therefore only they are taken into account in the presentation of the results. During a 5 mg infusion of ISDN arterial blood pressure showed a tendency to decrease. Left ventricular ejection time shortened (-3.9%) and the pre-ejection period lengthened (+ 21.9%). The pulmonary artery pressure showed minimal tendency to decrease. The right ventricular systolic time intervals showed a similar tendency but the changes were not significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Twenty-six men and women, aged 36-65 years, were studied 8-12 weeks after the first myocardial infarction with regard to silent ischemic ST-segment depression and heart rate by using 24-hour ambulatory electrocardiography and bicycle exercise testing. In 22 patients ambulatory ST-segment recordings revealed 81 episodes of ST-segment depression, including 34 (41.9%) painful and 47 (58.1%) painless episodes. Mean maximal ST-segment depression during symptomatic and asymptomatic episodes was 3.6 +/- 1.0 mm and 2.4 +/- 1.1 mm, respectively (p less than 0.02). Painless episodes most frequently occurred between 06.00 a.m. and 12.00 a.m. Ambulatory monitoring revealed a twofold increase in painful episodes at heart rate below 100 beats/min, whereas at heart rate above 125/min painless episodes were more frequent. Exercise testing showed a sevenfold increased incidence of ST-segment depression also at heart rate above 125 beats/min. In conclusion, silent myocardial ischemia is a frequent event in patients shortly after the first myocardial infarction, and painless episodes occur particularly frequently at high heart rates. Episodes of silent ischemia are found more frequently during ambulatory ECG monitoring than exercise testing. Studies on silent myocardial ischemia may be particularly relevant in the detection of the risk of myocardial infarction.

The response of the pulmonary circulation to captopril 75 mg has been examined in 21 patients with pulmonary hypertension secondary to mitral stenosis. The effects of captopril were measured every 15 min up to 2 h by recording pressures in the pulmonary and systemic circulations and by measuring cardiac output. Pulmonary artery systolic pressure fell significantly by 21.6% (from means = 54.6 to 42.8 mm Hg), pulmonary artery diastolic pressure by 23.3% (from 26.2 to 20.1 mm Hg), and the pulmonary artery mean pressure by 23.2% (from 36.9 to 28.3 mm Hg). Right ventricular end-diastolic pressure also fell significantly by 7% (8.1 to 7.5 mm Hg). Heart rate decreased by 6.5% (from 76.3 to 71.3 beats.min-1). Cardiac index and stroke volume index did not change. The total and vascular pulmonary resistance dropped significantly by 23.2% (from 721 to 553.7 dyn.s.cm-5) and 40% (from 287.2 to 172 dyn.s.cm-5), respectively. The right ventricular stroke work index fell by 33% (from 15.1 to 10.1 g/beat/m2). Systemic systolic pressure decreased by 10.5% (from 124.5 to 111.4 mm Hg). Thus, captopril lowered pulmonary pressures and resistances and no deterioration in right ventricular function was observed.

Myocardial blood flow in the region supplied by the right coronary artery was estimated in 36 patients after selective Xenon-133 injection into the artery. Its values were analyzed in relation to coronary driving pressure, diastolic coronary vascular resistance, and right ventricular triple product (tension-time index, TTI). Myocardial blood flow in the region supplied by the right coronary artery was increased in patients with moderately elevated pulmonary artery pressure (4.13 to 8.0 kPa; 31 to 60 mmHg). This increase was due to a significant lowering of diastolic coronary vascular resistance. In patients with severe pulmonary hypertension (above 8.00 kPa; >60 mmHg) the greatly increased value of TTI was not accompanied by a further augmentation of myocardial blood flow. This incommensurability between metabolic demand of the myocardium, reflected in TTI value, and the abililty to increase blood flow in the region supplied by the right coronary artery could be one of the causes of myocardial ischaemia and anginal pain in patients with extreme pulmonary hypertension.