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The antihypertensive and anti-ischaemic effects of methyldopa and captopril were compared in 12 hypertensive patients with coronary artery disease. The antihypertensive effect of alpha-methyldopa (A) and captopril (C) were significant and similar. On the other hand, while methyldopa did not increase the product of systolic pressure and heart rate and did decrease the effort-induced S-T segment depression, C increased the double product (DP) and decreased the ischaemic S-T changes. Captopril might be useful in the treatment of hypertensive patients with coronary artery disease.

The present study is focused on spectrum analysis as a useful method of processing the PCG in order to obtain the frequency spectral distribution of normal heart sounds. Thirty normal subjects aged from 17 to 34 were studied. PCG was recorded on the fourth intercostal space at the left sternal border using a sound level meter coupled with a standard 6 ml cavity. The microphone had a linear response from 0.2 to 8,000 Hz. The signal was filtered with the standard B network according to the ANSI specifications and was registered on a four track FM tape recorder. A four channel analyzer with a microprocessor for off-line elaborations was used with 10 KHz sampling frequency. The PCG signal was triggered by a QRS detector on the R wave of the simultaneously recorded ECG. Fast Fourier transform was performed employing either a four channel analyzer with a microprocessor, or an A/D converter with a computer. Finally the results of the analysis were statistically elaborated. The described procedures permit to obtain a direct and exact tracing of the acoustic features of the heart, thus representing an attempt to come closer to the standardization and automatic analysis of the phonocardiographic technique.

The anti-ischemic effect of a single oral dose of 10 mg of enalapril maleate (E) was investigated in 14 normotensive patients with coronary artery disease (CAD) and stable effort-induced angina pectoris. An exercise stress test was performed three times in each patient at the same clock hour on three successive days: with no treatment (baseline), 6 h after administration of placebo (P), and 6 h after oral administration of a single 10 mg dose of E. The multistage nonstop effort tests were performed in the sitting position. Workload started at 25 W and was increased by 25 W every 2 min until an ischemic ST depression of more than 1.5 mm was observed. The following parameters were measured: heart rate (HR), systolic blood pressure (BP), rate-pressure product (RPP), workload sustained (WS), elapsed time of effort (ET), and millimeters of ischemic ST depression. The values of the parameters observed with baseline, P, and E were compared at the moment of appearance of chest pain or ischemic ST depression, at the moment of maximal effort, maximal common WS (MCWS), and maximal common RPP (MCRPP). Enalapril delayed the appearance of the ischemic ST depression. At the MCWS, the RPP was significantly lower under E and the ST depression was less marked; this effect was the result of a lower BP level, in the absence of any significant change in HR response. The acute effects of E observed in normotensive patients with effort-induced angina pectoris seems to be related to the inhibition of angiotensin at the coronary level and to its antiadrenergic action.

A phonocardiographic study in a medium frequency range was made over various areas of the precordium in 27 cases of right bundle branch block (RBBB), 28 cases of left bundle branch block (LBBB), and 30 normal subjects of the same age. The various components of the first heart sound plus the pulses at the suprasternal notch and the right carotid artery were studied in regard to timing, relationship with the ECG and the arterial pulses, intervals between components, and amplitude. The timing and intervals of the three components of the first sound were found normal in RBBB and so were the arterial pulses; apparent wide splitting was occasionally noted, due to recording of the first (a) and third (c) components, the latter being larger, as frequently observed in old age. All three components of the first sound were found small and delayed in LBBB; a delay of the arterial pulses was also noted. No additional component that might be attributed to the right heart preceded the delayed first sound. This study confirms that the first heart sound recorded on the chest wall originates only in the left heart and aorta.

The modifications that atrial flutter determines on the phonocardiogram, apexcardiogram, carotid pulse tracing, jugular venous pulse tracing, and indirect (esophageal) left atrial pulse tracing were studied. On the basis of the data here presented and that of the literature, a polygraphic profile of atrial flutter has been constructed as follows: notable variability of the intensity and of the richness of the vibratory components of the first and second heart sound; regularly alternating intervals between successive atrial sounds, each one of which consists of two groups of vibrations; deformations of all mechanographic tracings corresponding with "F" waves of the ECG. The interpretation of various polygraphic reports contributes to the understanding of the physiopathogenesis of atrial flutter.

The first heart sound was studied in 20 normal subjects. The phonocardiogram (PCG) was recorded from apical and mid-precordial areas using microphone with a flat response curve from 0.2 to 8,000 Hz. It was stored, together with a simultaneous electrocardiogram, on an FM analog tape recorder (linear frequency response from 0 to 4,000 Hz), fitted with a filter with weighting curve B according to the American National Standard Institute. A linear (SPL) recording was also made. The signal was fed through a digital converter into a minicomputer and the frequency distribution of the first heart sound was analyzed using Fast Fourier Transform. These data were stored and the average spectra were calculated for both B and SPL. The SPL spectra from both apex and mid-precordium showed a maximum intensity of about 80 dB between 12-20 Hz, decreasing progressively to a constant level of 35 dB between 110-120 Hz. The spectra obtained from both areas using filter B showed a maximum intensity of 40-50 dB between 20-60 thereafter. It is important to emphasize that the dB values in B and SPL are absolute, since they refer to a standard reference weighting. It appears that the SPL recording is more valuable in that it allows the study of all components of the PCG signal. The spectra obtained in this study will be used as a standard for future research in various pathological conditions.

We investigated the effect of an orally administered, long-acting, beta-adrenergic blocking agent, penbutolol, on the circadian rhythm of blood pressure (BP) and heart rate (HR), and plasma renin activity (PRA), aldosterone (PA) and cortisol (PC) levels in hospital patients with essential hypertension validated by a chronobiological inferential statistic method. After a wash-out period of three weeks, a group of 8 hypertensive patients (5 women and 3 men, 27 to 41 years old) underwent automatic BP and HR monitoring, and blood sampling for 24 hours in a hospital room before and after 4 weeks of treatment with penbutolol (40-mg tablet once a day at 9 a.m.). In basal conditions, a statistically significant mean circadian rhythm was demonstrated for HR, diastolic BP, PRA, PA, and PC. Systolic and diastolic BP were lowered by penbutolol, with only a minor decrease of HR. The treatment eliminated also the mean circadian rhythm of BP and HR. Penbutolol induced both a remarkable reduction of PRA with disappearance of the related circadian rhythm and a significant decrease in PA levels with maintenance of their circadian rhythmicity. The circadian secretory patterns of PC were similar before and after therapy. In conclusion, long-term treatment with penbutolol appears not only to set BP, PRA and PA values to lower levels, but also to decrease the within-day variation of BP, HR, and PRA. In addition, penbutolol does not influence the 24 h-secretion of PC.

The amplitude of the pulmonic component of the second sound in aortic stenosis was studied in 49 patients with this lesion. As controls, 50 normal subjects were also studied. Both groups were investigated by phonocardiography, apex cardiography and arterial tracings. Nineteen patients with aortic stenosis and four subjects without it were also studied by cardiac catheterization and angiography. The amplitudes of the two components of the second sound were compared, and the ratio of each with the amplitude of the first sound was determined. The ratios of both the aortic and the pulmonic component to that of the first sound were decreased in aortic stenosis, and the decrease of the pulmonic component was comparable to that of the aortic component. These findings could be related to prolongation of the isovolumic relaxation period of both ventricles caused by an influence of the left ventricle on the right, most likely due to functional changes of the interventricular septum.

A study of relative bioavailability of two digoxin formulations was carried out on 28 healthy volunteer human subjects of both sexes. A commercial digoxin in tablet form was compared with a new commercial formulation which contains a solution of digoxin in soft gelatin capsules. The parameters investigated were: plasma levels, area under the plasma level-time curve, daily urinary excretion of digoxin and a series of polycardiographic measurements, all the parameters being evaluated in a steady-state condition (14 days of treatment). All the parameters investigated demonstrated better bioavailability in the capsules than in the tablets, the average improvement being 26.1%. The better bioavailability of digoxin capsules also resulted in more rapid and wider variations in the polycardiographic parameters.

The Authors briefly discuss the mechanism of production of the systolic click of mitral valve prolapse. A "valvular" mechanism seems inadequate to explain the genesis of vibrations that can be recorded, not only in the external phonocardiogram, but also in the intraventricular pressure tracing, in the apex cardiogram, and even in the left atrial pulse (esophagus). It seems more logical to postulate that the force of deceleration created by the sudden eversion of a mitral leaflet set the whole cardiohemic system (blood, myocardial walls, and the mitral apparatus) into vibration, thus producing the click. In mitral valve prolapse, the contribution to sound production of mitral leaflets and chordae is likely to be minor, as it had been demonstrated for the first heart sound.

The possibility of evaluating left ventricular function by noninvasive methods is discussed in detail. The methods that are considered are electrocardiograph, phonocardiography, apex cardiography, sphygmography, impedance cardiography, electrokymography, and echocardiography. Following a brief section of 'definitions', each method is described in detail including technical problems, difficulties, and results. The systolic time intervals and the stress tests are briefly discussed. Based on modern experimental studies, the stress test should include both an electro- and a phonocardiogram. In the latter, one would measure the amplitude of the first heart sound as an index of contractility. The conclusion is that combined methods give the best results. They are electrocardiography, phonocardiography, impedance cardiography, and echocardiography. An alternative, dictated by technical problems, is to use at first phonocardiography and impedance plus electrocardiography; then echocardiography plus electrocardiography; and then, if indicated, a stress test might complete the study; the latter should include both an electrocardiogram and a phonocardiogram.

The aim of this study was to investigate the effect of orally administered, slow-release, nifedipine tablets on the circadian rhythm of blood pressure and heart rate, in hospital patients with clinical diagnosis of hypertension validated by a chronobiologic inferential statistic method. A group of 14 patients (nine women and five men, 47 to 71 years old) with clinical diagnosis of "essential hypertension" underwent automatic blood pressure and heart rate monitoring in a hospital room for 48 hours. Measurements were taken every 15 min by an oscillometric instrument with automatically inflated cuff. The patients received no treatment during the two proceeding weeks and the first day of the study. On the second day, slow-release nifedipine tablets were administered, one at 10 a.m. and one at 10 p.m. A highly significant circadian rhythm was documented for systolic and diastolic blood pressure, mean arterial pressure and heart rate, both in basal conditions and after nifedipine. Blood pressure mesors were higher than reference standards in basal conditions, and were lowered (average decrease = 20 mmHg for systolic and 9 mmHg for diastolic mesor) by nifedipine. A significant, though minor, elevation of heart rate mesor (from 70 to 75 b.p.m.) was also noted during treatment. The circadian amplitudes of blood pressure and heart rate did not differ significantly before and during treatment. In conclusion, the circadian rhythm of blood pressure is still present with the same amplitude after slow-release nifedipine, but is set at a lower pressure level. Heart rate rhythm is also preserved, with only a minor elevation of its mesor.

Twenty-five patients suffering from mitral valve prolapse were studied to demonstrate any diagnostic modifications of the indirect (esophageal) left atrial pulse (ESO). Valvular prolapse is demostrated on the ESO by a sudden change in slope of the curve after the "x" point, in coincidence with a midsystolic click. Late systolic mitral insufficiency, when associated with prolapse is illustrated on the ESO tracing in two ways: a) an abnormally tall "v" wave; b) a late systolic plateau which begins immediately after the click and continues beyond the second heart sound. After the infusion of methoxamine or isometric exercise the ESO is usually of the a) conformation, while after the inhalation of amyl nitrite the tracing tends to be of the b) type. The "c" wave is at times altered but not always. This alteration is characterized by a greater amplitude and sharper peak. Based on the physiopathogenesis of the alterations of the ESO, it can be stated that they are specific, and sensitive enough to be both qualitative and quantitative.

The occurrence and extent of a circadian rhythm in the circulating concentrations of atrial natriuretic peptide (ANP) is still a matter of controversy. In a group of hospitalized normal volunteers (6 men and 4 women, 16-76 years old), we investigated the circadian variability of ANP and its temporal relation with the circadian rhythms of blood pressure (BP) and heart rate (HR), by using a chronobiological inferential statistical method. At the end of a synchronizing period of 1 week (the diet and the daily schedule were standardized), the subjects underwent automatic BP and HR monitoring, and blood sampling for 24 h. A statistically significant mean circadian rhythm was demonstrated for ANP, BP, and HR. The mean circadian acrophase of ANP was calculated to occur around 4 a.m. BP and HR rhythms appeared to be in antiphase with ANP rhythm, i.e. the peak of BP and HR rhythms more or less coincided with a trough in ANP rhythm. ANP appears to be anticipatory in its circadian periodic rise to awakening. Therefore, postural changes cannot fully account for the diurnal variations observed.

This is a retrospective study of 25 patients with secundum-type of ASD, confirmed by catheterization and angiocardiography. As controls, 25 normal subjects of matching age were studied. The phonocardiograms and carotid pulses of the 2 groups were recorded and compared. Special attention was paid to the interval between the 2 main components (Ia and Ib) of the first heart sound, to the amplitude of both Ia and Ib, and to the relationship between carotid upstroke and first heart sound. All intervals between sound components of the patients with ASD were found similar to those of the controls. No increase in amplitude of Ib could be documented. The amplitude of the first heart sound relative to that of the second sound (measured from the ratio I/IIA) was similar to that of the controls, Finally, a slight precedence of aortic valve opening (obtained from the carotid upstroke time minus transmission time) over the second component of the first sound (Ib) was found both in ASD and in controls. In view of these facts, a tricuspid contribution to the mechanism of the b component of the first heart sound appears highly unlikely. On the other hand, this component seems closely related to the dynamic events (blood acceleration and walls deceleration in the aortic root) that follow the aortic valve opening.

This report presents a rare case of isolated right ventricular infarction complicated by bilateral occlusive pulmonary embolism apparently due to right ventricular mural thrombus. Only 2 to 3 weeks later an infarct of the posterior wall of the left ventricle finally occurred. The clinical, pathological and electrocardiographic features of the case are discussed. This case shows that right ventricular infarct can occur without a preceding or simultaneous infarct of the left ventricle.

"Precordial honk" is a loud, high pitched, musical and usually intermittent systolic noise. The concept of extracardiac origin and "inocence" of this finding is superseded and today its valvular origin during mitral prolapse, mitral or tricuspidal insufficiency - due to rheumatic or ischaemic disease - or during cardiomiopathy is demonstrated. The acoustic characterization of this finding was based on phonocardiographic registration. All the authors describe the "precordial honk" as a high frequency murmur without specifying the acoustic characteristics of the phenomenon. A spectral analysis technique applied to the acoustic cardiac signal (Fourier analysis) has been employed in order to study the "precordial honk" of a 15-year-old boy with mitral valve prolapse. This made possible to show that this sound had only one fundamental frequency at 300 Hz. without harmonics; a "sea gull cry" murmur (as the cry of many birds is) justifying the name given by clinicians. The spectral analysis of phonocardiography signal allow to study, more precisely, the cardiac acoustic phenomenon.

The transmission delays of the upstroke and incisura of the arterial pulse were measured in 128 normal subjects, divided in three groups of increasing age, by comparing the timing of the indirect aortic arch pulse (recorded at the suprasternal notch) (SSN) and the indirect, right carotid tracing (CAR). In the total group, the mean delay of the upstroke was 24.4 msec while the mean delay of the incisura was 19 msec (P less than 0.005). This difference was maximal in the oldest age group and became non significant in the group of children under 12. At slow heart rate, this difference was greater than at a more rapid heart rate. The left ventricular ejection times (LVET), measured on the two pulses, showed a very close correlation (r = 0.96) but the LVET was significantly longer in the SSN tracing, especially in the older subjects. These data reveal that the incisura of the arterial pulse travels more rapidly than the upstroke, especially in older patients and at lower heart rates. The most likely explanation of this fact resides in the frequency-dependent influence of vascular reflections, which is more important with increasing age and slower heart rate. Thus, the transmission velocity along the arterial wall is higher for the higher harmonics of the pulse wave (incisura) than for the lower harmonics (upstroke).

The use of phonocardiography is limited by the lack of standardization of acoustical signal pick-up and of the filters. Moreover, quantitative evaluations are not possible. This limits the analysis of acoustic phenomena and makes confrontation between different laboratories impossible. To avoid these drawbacks we have developed a method based on phonometric principles. Heart sounds of twenty for normal subjects were recorded by an air-coupled microphone with the standard 6 ml cavity. The response curve of the microphone is flat from .2 to 8000 Hz. The signal was measured and stored on an analogic tape recorder together with the ECG. For each subject the 3 weighting networks (A, B and C, according to the American National Standard Institute) and the linear recording (SPL) were used and the peak value of every record was written down in dB-peak. The amplitude spectra were obtained through the FFT algorithm. Normal heart sounds reached a high frequency limit of 170 Hz. with a maximum amplitude of 67 dB SPL, 24 dB A, 42 dB B and 59 dB C. Each spectral pattern can provide a useful reference to compare with pathological acoustical findings.

Non invasive blood pressure monitoring using an automatic Nippon Colin recorder was performed in 20 hospitalized hypertensive patients every 15 min during a 4-day study period. A chronobiologic analysis of the data was performed in order to test the consistency of the whole-day blood pressure pattern. Halberg's method of single cosinor was used to determine the values and the confidence limits of the following parameters of 24-hour rhythmic changes: mesor (rhythm-adjusted 24-hour average), amplitude (24-hour variability estimate), acrophase (clock hour of maximum BP level). The variation of the above parameters during the four 24-hour periods was found to be within 9 mmHg for the systolic mesor, 6 mmHg for the diastolic mesor, 5 mmHg for the systolic amplitude, 4 mmHg for the diastolic amplitude, 55 min for the systolic acrophase, 60 min for the diastolic acrophase. The same parameters were also calculated in 48-hour, 72-hour and 96-hour long time series, and with different sampling periods (30, 60, 120 min). The length of the monitoring span did not influence significantly the values of the rhythm parameters only when 15-min or 30-min sampling periods were used. The widths of the 95% confidence limits of amplitude and acrophase were significantly narrower in the 2-day than in the 1-day series. Further lengthening of the monitoring span from 2 to 4 days resulted in a much smaller additional narrowing of the confidence limits. Sampling periods longer than 30 min caused a loss of sensitivity in rhythm detection.(ABSTRACT TRUNCATED AT 250 WORDS)

The diagnostic usefulness of the indirect (esophageal) left atrial pulse (ESO) has been analyzed in: 1) 25 patients (pts) with mitral insufficiency (MI), 2) 18 pts with mitral stenosis, 3) 29 pts with combined valvular disease, 4) 10 normal subjects. In addition, in 1) and 4), the ESO was recorded under the following dynamic conditions: a) during isometric exercise (handgrip), b) after inhalation of amyl nitrite, c) after intravenous infusion of methoxamine. The ESO tracing demonstrated estimates of the severity of the disease. Under dynamic conditions no modification from the resting morphology was obtained in the control group, whereas in MI the following modifications were observed: a) increased, progressive, positive elevation of the systolic phase of the ESO during the handgrip and the administration of the methoxamine; b) tendency to return to normal morphology after amyl nitrite.

Twelve normotensive patients with coronary artery disease and stable effort-induced angina pectoris were selected: the antiischemic effect of captopril was studied. A maximal cycloergometer effort test was obtained before (base) and after administration of placebo or captopril (50 mg p.o.). The following parameters were measured: heart rate (HR), blood pressure (BP), maximal rate/pressure product (MRPP), maximal workload sustained, (MWS), maximal working time (MWT), and S-T depression at MRPP. The base and placebo were similar. Compared to them captopril augmented the MWT, increased the MWS, reduced S-T depression at MRPP, and decreased the number of patients with effort-induced angina pectoris. The antiischemic effect of captopril seems related both to its effect on HR and BP, and to a local enhancement of coronary blood flow.