Normal electrophysiological findings in a patient with symptomatic intermittent advanced atrioventricular block.

This report describes an otherwise healthy young woman who presented with syncope during episodes of advanced atrioventricular (AV) block. The His bundle recordings during normal sinus rhythm and atrial and ventricular pacing were normal. Carotid sinus massage produced no abnormality. Subsequently, the patient received a permanent pacemaker and has been free of symptoms. Intermittent advanced AV block has been observed on follow-up electrocardiograms. This unique case demonstrates a potential limitation of routine electrophysiologic investigation.

Can the human right ventricle create a negative diastolic pressure suggestive of suction?

Pressure in the right ventricle (RV) as well as the right atrium (RA) and pulmonary artery (PA) were measured in 80 patients with catheter-tip micromanometers and evaluated to determine if the pressures are compatible with the concept of RV diastolic suction. In 40 patients with normal PA pressure, minimal RV diastolic pressure that occurred during early filling, was negative (-2 +/- 0.3 mm Hg) (mean +/- SEM). In 29 patients with PA hypertension, minimal RV diastolic pressure during expiration also was negative (-2 +/- 0.7 mm Hg). In 11 patients with right ventricular failure, however, minimal RV diastolic pressure was positive (9 +/- 2 mm Hg). These results indicate that the human right ventricle, in the absence of failure, has a negative early diastolic pressure, which may reflect RV diastolic suction.

Effect of chronic pressure overload on the maximal rate of pressure fall of the right ventricle.

The maximal rate of fall in right ventricular pressure (negative dp/dt) was evaluated in 34 patients. Eight had normal pulmonary arterial pressure. Seventeen had pulmonary arterial hypertension, and nine had pulmonary arterial hypertension with right ventricular failure. The right ventricular maximal negative dp/dt in patients with normal pulmonary arterial pressure was 170 +/- 20 mm Hg/sec. In patients with pulmonary arterial hypertension not accompanied by right ventricular failure, this value was 670 +/- 60 mm Hg/sec; and in patients with right ventricular failure, it was also 670 +/- 60 mm Hg/sec. This was higher than in control subjects (P less than 0.001). The maximal positive dp/dt was also higher in patients with pulmonary hypertension, regardless of the presence of right ventricular failure. Right ventricular maximal negative dp/dt correlated with right ventricular maximal positive dp/dt (r = 0.72). Right ventricular maximal negative dp/dt in patients who were not in right ventricular failure correlated linearly with pulmonary arterial systolic pressure (r = 0.83) and pulmonary arterial diastolic pressure (r = 0.83). At any level of pulmonary arterial systolic pressure, right ventricular maximal negative dp/dt in patients with right ventricular failure was lower than in patients with the same level of pulmonary arterial hypertension who were not in failure. These observations indicate that right ventricular maximal negative dp/dt is dependent on load. Even in the presence of right ventricular failure, right ventricular maximal negative dp/dt exceeded values in control subjects.

Effect of turbulent blood flow on systolic pressure contour in the ventricles and great vessels: significance related to anacrotic and bisferious pulses.

The effect of turbulent blood flow on the contour of systolic pressure in the left and right ventricles and great vessels was investigated in 64 patients undergoing diagnostic cardiac catheterization. Intracardiac pressure and sound were recorded using a catheter-tip micromanometer. Measurements were made in normal subjects and patients with a variety of disorders including aortic stenosis, hypertrophic obstructive cardiomyopathy, coarctation of the aorta and atrial septal defect. Observations showed a consistent association of the intracardiac murmur, which is indicative of turbulence, with a transient reduction of the centrally recorded systolic pressure. The resultant abnormal systolic pressure contour can be explained on the basis of fluid dynamic considerations related to turbulence.

Negative intraventricular diastolic pressure in patients with mitral stenosis: evidence of left ventricular diastolic suction.

Left ventricular diastolic pressure was evaluated in 15 patients with mitral stenosis and 16 patients with no significant heart disease to determine if a stenotic mitral valve can cause the left ventricle to produce a negative diastolic pressure, indicative of ventricular diastolic suction. The minimal level of diastolic pressure in patients with mitral stenosis ranged between 6 and -7 mm Hg; in normal subjects it did not fall below 0. The average value of minimal diastolic pressure in patients with mitral stenosis (-2 +/- 1 mm Hg [mean +/- standard error of the mean]) was significantly lower than in patients without significant heart disease (5 +/- 1 mm Hg) (p less than 0.001). These observations indicate that the human left ventricle, in the presence of mitral stenosis, can generate a negative diastolic pressure. The presence of a negative diastolic pressure in patients with mitral stenosis suggests that the dynamics of the ventricle during diastole may contribute to the filling process.

Mid-systolic closure of the aortic valve in hypertrophic obstructive cardiomyopathy: a pressure-related phenomenon induced by turbulent blood flow.

The purpose of this study was to determine whether mid-systolic closure and opening of the aortic valve in patients with hypertrophic obstructive cardiomyopathy (HOCM) may reflect dynamic changes of pressure induced by turbulent blood flow in the aorta and left ventricular outflow tract. Five patients with HOCM who had echocardiographic evidence of mid-systolic closure of the aortic valve and two patients with HOCM who did not have transient mid-systolic closure of the aortic valve were studied. In patients in whom mid-systolic closure was present, a transient mid-systolic drop of pressure was present in the left ventricular outflow tract, distal to the dynamic intraventricular obstruction, 17 +/- 3 mm Hg (mean +/- SEM) and in the root of the aorta, 16 +/- 4 mm Hg. In these patients the mid-systolic drop of pressure was consistently associated with a high-intensity intracardiac murmur indicative of turbulence. In the two patients in whom mid-systolic closure of the aortic valve was absent, the transient mid-systolic drop of pressure during systole was minimal (average, 3 mm Hg). The transient mid-systolic drop of pressure distal to the intraventricular obstruction can be explained on the basis of decreased pressure energy of the blood due to turbulence. Since total energy is conserved, increased kinetic energy due to turbulence occurs at the expense of a loss in pressure energy. The transient mid-systolic reduction of pressure in the turbulent zone during systole may cause a pressure differential across the open valvular leaflets resulting in a transient closure of the aortic valve.

Orifice-view aortography in patients with congenitally deformed aortic valves: determination of aortic valve area.

Orifice-view aortography is a contrast cineaortographic technique that allows en face viewing of the aortic valve. In this projection the anatomic configuration of the aortic valve is identified, and it is possible to planimeterize the visualized aortic valve opening and accurately determine the orifice area. Fifteen individuals with congenitally deformed aortic valves with gradients ranging from trivial (< 10 mm Hg) to surgically significant (6E 60 mm Hg) were subjected to aortic orifice area measurement by orifice-view aortography, and the area was compared with the peak systolic gradient and valve area. The results yielded a cloe correlation with the aortic valve area index as measured hydraulically or, as in three instances, directly from the surgically excised specimen (r = 0.94). A satisfactory correlation was also shown with the valve area index and the peak aortic valve gradient (r = 0.85). These observations indicate that orifice-view aortography is an accurate method for the measurement of the aortic valve orifice and may be particularly useful when hydraulic measurements are unattainable or invalid.

Intracardiac sound as a diagnostic adjunct in subaortic stenosis.

The purpose of this investigation is to demonstrate the potential diagnostic value of intracardiac sound recordings in patients with subaortic stenosis. Intracardiac pressure and sound were measured in 10 patients with various types of subaortic obstructions using a catheter-tip micromanometer. Seven patients had idiopathic hypertrophic subaortic stenosis (IHSS), 2 had a subvalvular membrane, and 1 had a subvalvular tunnel. Within the left ventricular cavity, at the site of maximal systolic left ventricular pressure, either there was no systolic murmur, or the murmur was of low intensity. However, within the outflow tract of the left ventricle, distal to the site of intraventricular obstruction, a prominent systolic murmur was detected in all patients. This murmur was of higher intensity than the one measured distal to the aortic valve. In one patient, in whom no subvalvular obstruction was present, but in whom entrapment of the tip of the catheter occurred, no murmur was detected in the left ventricle even though a subvalvular pressure gradient was observed. Therefore it appears that a systolic murmur recorded with maximal intensity in the outflow tract of the left ventricle may be of substantial help in distinguishing between an artifactual intraventricular pressure gradient, and one that results from intraventricular obstruction.

Performance of the failing and nonfailing right ventricle of patients with pulmonary hypertension.

Hemodynamic performance of the right ventricle was measured in 34 patients: 17 with pulmonary hypertension, 9 with pulmonary hypertension and right ventricular failure and 8 control subjects. Among the patients with pulmonary hypertension who did not have right ventricular failure, right ventricular maximal isovolumic rate of development of ventricular pressure (dP/dt) was significantly elevated (P less than 0.001), whereas maximal 1/P dP/dt and maximal velocity of contractile element shortening (Vmax) were comparable with values observed in control subjects. The patients with pulmonary hypertension who had right ventricular failure also showed an augmented right ventricular maximal dP/dt (P less than 0.001) and normal 1/P dP/dt and Vmax. These observations indicate that in pulmonary hypertensive heart disease, even when the right ventricle failed in a clinical sense, the contractile effort was normal. Consequently, right ventricular failure may develop in patients with pulmonary hypertensive heart disease even though the cardiac muscle performs normally as a contractile tissue.

Diagnostic value of visualization of the right ventricle using thallium-201 myocardial imaging.

The diagnostic significance of visualizing the right ventricle on thallium-201 myocardial perfusion scans (T-scan) at rest was studied in 53 patients. In 33 patients the right ventricle was visualized clearly on the T-scan (group A). Hemodynamic evidence of right ventricular hypertension with systolic pressure greater than or equal to 30 mmHg was present in 28 of 33 (85%) of these patients. Right ventricular volume overload with left-to-right shunt greater than 2:1 was present in three patients. Other tests were diagnostic for right ventricular enlargement and or pulmonary hypertension as follows: chest x-ray (58%), echocardiogram (36%) and electrocardiogram (15%). In an unselected group of 20 patients (group B) where resting T-scan did not show visualization of the right ventricle, the right ventricular systolic pressure was less than 30 mm Hg in all. The other noninvasive tests did not reveal presence of right ventricular hypertrophy or enlargement. T-scan appears to be a useful and sensitive test in detecting right ventricular pressure or volume overload compared with other noninvasive tests. This may be useful in detection of patients with right ventricular hypertrophy or enlargement secondary to pulmonary hypertension or other causes.

Exploration of the cause of the low intensity aortic component of the second sound in nonhypotensive patients with poor ventricular performance.

This investigation was undertaken to explore the cause of the diminished second sound (S2) that may occur in normotensive patients with poorly performing ventricles. Intra-aortic sound and pressure were measured in 16 patients with angina; eight had normal ventricular performance (ejection fraction greater than or equal to 60%) and eight had poor performance (ejection fraction less than 50%). The amplitude of S2 was lower in patients with poor ventricular performance as was negative d/dt. Aortic pressure was conparable in both groups. The ampitude of S2 was linearly related to the rate of change of the pressure gradient that developed across the aortic valve during diastole (r = 0.82). The latter also correlated with negative dp/dt (r = 0.82). These observations indicate that in patients with poor ventricular performance, isovolumic relaxation may be compromised. This would cause a reduction of the rate of development of the diastolic pressure gradient, which would result in a diminished S2.

Significance of momentary pressure changes during isovolumic relaxation.

Sudden momentary fluctuations of left ventricular, aortic, right ventricular, and pulmonary arterial pressure were noted during isovolumic relaxation of the respective ventricles. The presence of such transients raised questions related to their meaning and significance. The purpose of this report is to emphasize the nonartifactural nature of these pressure transients and to describe their origin and significance in the cardiac cycle. Pressure transients were observed in 31 of 32 patients with normal aortic valves, and in 17 patients with normal pulmonary valves in whom right-sided measurements were made. Such transients, however, were absent on the left ventricular and aortic pressure recordings of three patients with calcific aortic stenosis. These sudden changes in pressure are indicative of momentary compressions and rarefactions of the blood that occur within the ventricles and their respective arterial chambers. Whenever present, pressure transients were noted to occur coincident with the major aortic or pulmonary components of the second sound. Since intraaterial sound pressure is derived from the pressure signal by litering the low frequencies and amplifying the high frequencies, one can deduce that intraarterial sound pressure is in fact a representation of these pressure changes. The recognition of these pressure transients on an otherwise smooth ventricular, aortic, or pulmonary arterial pressure places in proper perspective their role in the production of the second heart sound.

The aortic closure sound in pure aortic insufficiency.

The second sound in aortic insufficiency has been described as accentuated, normal, or moderately diminished. A study of intracardiac phonocardiograms was performed to evaluate its intensity and to eliminate extracardiac factors. Pressure and intracardiac sound measurements were made in 28 patients undergoing diagnostic cardiac catheterization. Recordings were obtained above the aortic valve and within the left ventricle in 14 patients with normal aortic valves and 11 patients with aortic insufficiency uncomplicated by aortic stenosis. The amplitude of the aortic closure sound in the patients with pure aortic insufficiency, 1000 +/- 100 dynes/cm2, was significantly lower than in those patients with normal aortic valves, 3100 +/- 200 dynes/cm2 (P less than 0.001). The results indicate, therefore, that the presence of aortic insufficiency causes a diminished amplitude of the aortic closure sound. These results are supportive of the theory that the second heart sound is caused by diastolic vibrations of the closed aortic cusps. Diminished valvular vibrations and sound would occur in pure aortic insufficiency if the valve is unable to properly tense during diastole, or if the rate of development of the driving pressure is diminished.