Investigation of symptom free patients after myocardial infarction

The dicrotic pulse is an abnormal carotid pulse found in conjunction with certain conditions characterised by low cardiac output. It is distinguished by two palpable pulsations, the second of which is diastolic and immediately follows the second heart sound. In the course of open chest canine studies of the second heart sound, micromanometers and an electromagnetic flow meter were used to study proximal aortic haemodynamic function in both strong and weak beats. It was found that the incisural notch of the aortic pressure signal is not strongly dependent on the extent of left ventricular ejection, and is of essentially normal amplitude even in beats having greatly reduced aortic flow. In contrast, the magnitude of the systolic upstroke of the aortic pressure pulse is strongly determined by the magnitude of left ventricular ejection and is considerably reduced in weak beats. With low cardiac output the relative size of the incisural notch becomes exaggerated in comparison with the overall pulsation, thus creating the characteristic M shaped waveform of the dicrotic pulse.     

Characterization of left ventricular external wall motion in man by video dimension analyzer (Vidian)

Several investigators have described close relationships between left ventricular wall motion and physiologic cardiac events. Using an improved wall motion tracking devide (Vidian) in studies of 30 patients, we have compared the dynamics of left ventricular wall motion, recorded noninvasively, with high fidelity left ventricular and aortic pressures, intracardiac phonocardiograms, apexcardiograms, and cyclic left ventricular volume curves obtained during cardiac catheterization. Wall motion tracking signals comprised: pre-ejection outward deflection commencing with the first component of the first heart sound and coincident with the pre-ejection phase of the left ventricular pressure and apexcardiogram; a sharp descent during ejection, commencing with the ?E”? point of the apexcardiogram and with the onset of the upstroke of the aortic pressure; end ejection nadir, synchronous with the dicrotic notch of the aortic pressure; a nadir representing cessation of inward displacement, presumably reflecting slight inertial motion of the wall; a brief period of isovolumic relaxation which terminated synchronously with the ?O”? point of the apexcardiogram; rapid, then slow filling waves, coincident with those of the apexcardiogram, and demarcated by a transitional angulation synchronous with the third heart sound; and ?a”? wave, occurring simultaneously with that of the apexcardiogram. Ventricular wall motion tracking signals also corresponded to curves representing cyclic changes in left ventricular minor radius, and chamber volume derived from cineventriculograms. In 10 patients with abnormal contraction patterns detected by biplane cineventriculography, anomalous deflections were also recorded during ejection by the Vidian. Left ventricular wall motion tracking with the Vidian: 1) provides a sensitive index for timing of intracardiac events, 2) reflects cyclic changes in ventricular volumes and minor dimensions, 3) provides a convenient noninvasive technique for detection of regional asynergy involving the lateral left ventricular wall, and 4) by correlation with simultaneous ventricular pressure measurements, may provide useful information regarding left ventricular pressure/segment dimension relations.     

Experimental cardiac tamponade: a hemodynamic and Doppler echocardiographic reexamination of the relation of right and left heart ejection dynamics to the phase of respiration

A hallmark of cardiac tamponade is pulsus paradoxus. However, the exact mechanism of pulsus paradoxus and the relation of left and right ventricular ejection dynamics remain controversial, with some studies suggesting an inverse relation in ventricular filling and ejection and others citing a more important role for the effects of right heart ejection dynamics delayed by transit through the pulmonary artery bed. To specifically reexamine this issue, six sedated but spontaneously breathing dogs were studied during experimental cardiac tamponade with use of extensive hemodynamic instrumentation and Doppler methods. During cardiac tamponade, left ventricular systolic pressure decreased from 125.8 +/- 12.1 to 81.7 +/- 26.7 mm Hg (p less than 0.01) and cardiac output from 5.86 +/- 1.48 to 2.34 +/- 0.98 liters/min (p less than 0.001); mean pericardial pressure increased from -1.2 +/- 0.8 to 10.5 +/- 3 mm Hg (p less than 0.001) and pulsus paradoxus from 4.3 +/- 1.6 to 10.7 +/- 1.2 mm Hg (p less than 0.001) compared with baseline values. An inverse relation in left and right ventricular ejection dynamics that was very close to 180 degrees out of phase was seen throughout the respiratory cycle in multiple hemodynamic and Doppler variables including peak systolic pressures, aortic and pulmonary flow velocities and ventricular ejection times. Simultaneous recording of the transmitral pressure gradient provided indirect evidence that the ventricular ejection dynamics were directly related to changes in ventricular filling. However, the magnitude of ventricular pressure or output flow velocity for each respiratory cycle was variable, depending on the exact timing of filling and ejection in relation to the phase of respiration. Variation in left ventricular output due to changes in right ventricular output delayed by transit through the pulmonary vasculature was not recognized in any animal. It is concluded that in spontaneously breathing dogs with acute cardiac tamponade, peak ventricular pressures, ventricular ejection times and pulmonary and aortic flow velocities have an inverse relation that is very close to 180 degrees out of phase.     

Time course of pressure and flow in ascending aorta during ejection.

To analyze aortic flow and pressure relationships, 10 closed-chest anaesthetised dogs were instrumented with electromagnetic aortic flow probes and micromanometers in the left ventricle and ascending aorta. Left ventricular ejection time was divided into: time to peak flow (T1) (both pressure and flow rising), peak flow to peak pressure time (T2) (pressure rising, flow decreasing), and peak pressure to dicrotic notch time (T3) (pressure and flow both decreasing). These time intervals were expressed as percent of total ejection time. Load-active interventions rose markedly T2 (from 4.2 +/- 5.5 to 19.4 +/- 3.5 after phenylephrine (p less than 0.02); from 4.2 +/- 6.5 to 21.2 +/- 5.3 after dextran (p less than 0.02)). Conversely, dobutamine reduced T2 from 4.4 +/- 5.9 to -2.5 +/- 6.5 (p less than 0.05). Thus, during load-active interventions aortic pressure increases for a longer T2 time although forward flow is decreasing, as a result of higher aortic elastic recoil during ejection. Conversely, beta 1-adrenergic stimulation significantly shortens T2. Dynamic pressure-flow relationship is thus continuously changing during ejection. T2 seems to be inversely related to the efficiency of left ventricular ejection dynamics.     

Timing of the carotid arterial sounds in normal adult men: measurement of left ventricular ejection, pre-ejection period and pulse transmission time

The first and second carotid arterial sounds (CaS1 and CaS2) were recorded simultaneously with the aortic valve echocardiogram, carotid pulse wave contour, heart sounds, and electrocardiogram in 27 healthy, normal subjects. The mean intervals between the onset of the QRS complex and the onsets of the first and second major components of the carotid arterial sounds were Q-CaS1 = 131 +/- 15 ms and Q-CaS2 = 412 +/- 36 ms, respectively. The mean delay of CaS1 after aortic valve opening was 43 +/- 6 ms, while the delay of CaS2 after aortic valve closure was 43 +/- 7 ms. The onset of CaS1 and CaS2 are exactly coincident with the upstroke and with the dicrotic notch of the carotid pulse wave contour. The recording of the carotid arterial sounds, heart sounds, and ECG has enabled us to measure systolic time intervals including the pre-ejection period, left ventricular ejection time, and pulse transmission time more easily than using the conventional method involving the carotid arterial pulse wave contour. The new approach provides accuracy and precision comparable to that of the previous methods.     

Left ventricular end-systolic pressure-volume relation: A combined radionuclide and hemodynamic study

This study examines the effect of increasing heart rate by atrial pacing on the left ventricular endsystolic pressure-volume relation and determines whether peak pressure can be used instead of end-systolic pressure. Measurements were made of cardiac output (by thermodilution), pulmonary arterial pressure, ejection fraction (by radionuclide angiography), and aortic pressure (by intraarterial catheter). End-systolic pressure was measured at the dicrotic notch. The end-diastolic and end-systolic volumes were determined from the ejection fraction and cardiac output. There was excellent correlation in pressure-volume relation determined by peak pressure and end-systolic pressure (r = 0.95). In 8 normal subjects there was < 5% change in ejection fraction, a decrease in end-systolic volume, ≥ 30% increase in end-systolic pressure/ end-systolic volume, and no change in pulmonary arterial pressure with pacing. Of 20 patients with coronary artery disease, 9 patients had ≥ 5% decrease in ejection fraction, 6 had an increase in end-systolic volume, and 14 had < 30% increase in end-systolic pressure/end-systolic volume with pacing (p < 0.05). Thus (1) peak systolic pressure can be used reliably instead of end-systolic pressure; (2) atrial pacing has a positive inotropic effect in normal subjects—the minimal increase (30%) in end-systolic pressure/end-systolic volume is similar to the increase (35%) reported during exercise; (3) abnormal changes in end-systolic pressure/end-systolic volume in coronary artery disease are more common than changes in either ejection fraction or end-systolic volume with atrial pacing.     

Hemodynamic effects of acute atrioventricular sequential pacing in patients with left ventricular dysfunction

Acute atrioventricular (A-V) sequential pacing was compared with ventricular pacing in seven men with symptomatic left ventricular failure (New York Heart Association functional class III and IV) and depressed left ventricular ejection fraction (mean 29 percent, range 18 to 40). Cardiac index was higher during A-V sequential pacing than during ventricular pacing for every patient at paced rates of 75 to 100 beats/min. The mean increment was 17 percent (range 10 to 37) at a paced rate of 75 beats/ min, 23 percent (range 8 to 45) at a paced rate of 85 beats/min and 29 percent (range 19 to 55) at a paced rate of 100 beats/min. The increase in cardiac index in an individual patient did not correlate with baseline characteristics including functional class, cardiothoracic ratio, resting ejection fraction, cardiac index or balloon-occluded pulmonary wedge pressure.Arterial pressure varied from beat to beat during ventricular pacing because of the changing relation of atrial to ventricular systole. When an atrial contraction preceded a ventricular paced beat by a physiologic interval intraarterial pulse pressure uniformly increased. That increase correlated strongly (r = 0.993) with the increase in cardiac index that occurred during A-V sequential pacing. Measurement of the pulse pressure during A-V dissociation is a simple technique that may be useful for predicting the degree of improvement in cardiac output expected with methods of pacing that restore A-V synchrony.     

Influence of sublingual nitroglycerin on the digital circulation of man

By means of the digital rheoplethysmographic (RPG) method, the effect of sublingually administered nitroglycerin (NTG), 1/200 gr (0.3 mg), on the digital circulation was studied in 17 normal subjects and 5 patients with ischemic heart disease and angina pectoris. NTG produced dilatation of all digital vessels, reflected especially by increases in total digital volume. NTG produced marked changes in the dicrotic notch of the pulse wave, noted also in inflow volume curves but not in outflow volume curves. The dicrotic notch was displaced later on the descending limb of the digital pulse wave and became deeper and more prominent after NTG. It is suggested that NTG produces disproportionate dilatation of the arterial system, having its greatest effect on arteries near the heart, including the coronaries and great vessels branching off the aorta, and on left intraventricular cavity pressure. This greater regional vasodilatation of vessels near the heart could delay closure of the aortic valve, producing a delayed and prominent dicrotic notch of the pulse wave.     

Effect of ventricular function on left ventricular ejection time in aortic stenosis

Since recognition of factors which modify the duration of ejection in aortic stenosis is of clinical importance, the relations among rate-corrected left ventricular ejection time, aortic valve area, and determinants of ventricular performance were studied in 54 catheterised patients. In patients with a normal cardiac index, increasing duration of ejection was linearly related to increasing obstruction. In patients with failing ventricles, on the other hand, the ejection time was less prolonged, and the duration of ejection was unrelated to valve area. At fixed valve area, relation with cardiac output, stroke volume, heart rate, mean aortic valve pressure gradient, mean aortic pressure, and left ventricular end-diastolic pressure could not adequately explain the observed scatter in ejection time. This suggests a multifactorial basis for the wide range of ejection times observed with severe aortic stenosis.     

Effect of ventricular function on left ventricular ejection time in aortic stenosis.

Since recognition of factors which modify the duration of ejection in aortic stenosis is of clinical importance, the relations among rate-corrected left ventricular ejection time, aortic valve area, and determinants of ventricular performance were studied in 54 catheterised patients. In patients with a normal cardiac index, increasing duration of ejection was linearly related to increasing obstruction. In patients with failing ventricles, on the other hand, the ejection time was less prolonged, and the duration of ejection was unrelated to valve area. At fixed valve area, relation with cardiac output, stroke volume, heart rate, mean aortic valve pressure gradient, mean aortic pressure, and left ventricular end-diastolic pressure could not adequately explain the observed scatter in ejection time. This suggests a multifactorial basis for the wide range of ejection times observed with severe aortic stenosis.     

Noninvasive estimation of left ventricular end-systolic pressure

A method for noninvasively determining left ventricular (LV) end-systolic pressure (ESP) using carotid pulse tracings and cuff-measured blood pressure was re-evaluated. It was validated during diagnostic cardiac catheterization in 60 patients with cardiovascular diseases. LVESP calculated by this method and systolic blood pressure measured by the cuff were compared with aortic dicrotic notch pressures obtained by a catheter-tip manometer system as true LVESP. The calculated ESP was measured by the following formula; [the ratio of the excursion of dicrotic notch (b) to the peak (a) in carotid pulse tracings: (b/a) x pulse pressure] + diastolic blood pressure. This calculated ESP had a high correlation coefficient with true ESP invasively measured (r = 0.96), but was estimated to be 5.3 +/- 5.0 mmHg less than true ESP. Systolic blood pressure, used as a noninvasive index of ESP, accurately estimated ESP, but it was higher by 14.8 +/- 11.2 mmHg (r = 0.84). Calculated ESP measured by the present method was not affected by age or systemic vascular resistance. This is a reliable noninvasive means of estimating LV end-systolic pressure. Compared with the peak arterial pressure, this is a better parameter for the analysis of LV contractility, such as stress-shortening, and end-systolic pressure-volume relations.     

Frequency analysis approach to the origin of the first and second heart sounds

Catheter-tipped micromanometers were used to simultaneously record left ventricular and aortic pressures, and left ventricular and aortic internal phonocardiograms in order to determine if they had a common mode of origin and propagation. Spectrographic analysis showed that even with high-pass filtration the phonocardiogram obtained with a commonly used system (Millar) contained large amounts of energy in the subaudible frequency range (below 40 Hz). It was possible to derive close facsimiles of the phonocardiograms by double differentiation of the corresponding pressure pulse and conversely to derive the pressure pulse by double integration of the phonocardiograms. The propagation velocities of the first heart sound, second heart sound, and the foot of the aortic pressure pulse were found to be similar and were respectively, 4.3 ± 0.2, 4.6 ± 0.3, and 4.2 ± 0.2 m/sec (± SE). These data support the concept that the low frequency pressure variations produced by the heart, which predominate in the left ventricular and aortic pressure pulse waveforms, are generated and propagated in the same manner as the high frequency pressure variations, which are the first and second heart sounds.     

Noninvasive beat to beat monitoring of left ventricular function by a nonimaging nuclear detector during premature ventricular contractions

A specially designed cardiac probe was used to evaluate beat to beat changes in left ventricular performance caused by premature ventricular contractions in four open chest dogs and 15 patients with various cardiac disorders. After intravenous injection of 15 to 20 mCi of technetium-99m serum albumin, left ventricular time-activity curves were obtained by positioning the probe over the left ventricular area in a 40 ° lateral anterior oblique projection with a 10 to 20 ° caudad tilt. Correct positioning was found by maximizing both the stroke counts and the end-diastolic counts. In the animal experiments, data generated by the probe were displayed side by side with left ventricular pressure, aortic pressure and aortic flow. Increases or decreases in stroke volume measured with the flowmeter correlated well with those measured with the cardiac probe. In the patients, the relative standard deviation of filling volumes, stroke volumes and ejection fractions of the sinus beats was 16 ± 5 percent, 14 ± 5 percent and 12 ± 5 percent, respectively. The premature ventricular contractions manifested end-systolic volume greater than, equal to or less than that of sinus beats. The filling volume, stroke volume and ejection fraction of these contractions were 51 ± 21 percent, 57 ± 17 percent and 45 ± 19 percent lower, respectively, than those of the sinus beats. In the compensatory sinus beats stroke volume and ejection fraction were 20 ± 27 percent and 26 ± 12 percent higher, respectively, than those in the sinus beats; however, the filling volume of these beats was essentially equal to that of the sinus beats.     

Acute and chronic effects of nicardipine on systolic and diastolic left ventricular performance in patients with heart failure: a pilot study

Nicardipine is a new calcium ion antagonist with vasodilating properties which has been shown to be effective in the treatment of hypertension and angina. We have studied its effect on systolic and diastolic left ventricular function in patients with mild to moderate degrees of congestive heart failure. Ten male patients with New York Heart Association Class II and III heart failure underwent acute treatment with an intravenous infusion of nicardipine (10 mg over 10 minutes). A nuclear probe was used to monitor left ventricular ejection fraction, peak filling rate, and relative cardiac output. Blood pressure and heart rate were also measured. The blood pressure (mean +/- SD) fell from 133 +/- 26/86 +/- 11 mmHg to 103 +/- 22/69 +/- 13; the heart rate rose from 67 +/- 9 beats/min to 85 +/- 10; left ventricular ejection fraction from 31 +/- 7 to 38 +/- 6%; relative cardiac output from 24 +/- 9 to 41 +/- 11; peak filling rate from 1.18 +/- 0.4 end-diastolic volume per second to 1.82 +/- 0.4 (p less than 0.001 in all cases) at the end of infusion. After 4 weeks of chronic treatment in eight patients (20 mg to be taken three times daily (tds) in one and 40 mg tds in 7), the blood pressure and heart rate had returned to baseline values but the improvements in left ventricular ejection fraction, relative cardiac output, and peak filling rate were sustained; this was associated with functional improvement in all 8 patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

Influence of the aortic component of the second heart sound on left ventricular maximal negative dP/dt in the dog

Maximal negative left ventricular dP/dt is widely used as a measure of isovolumic muscular relaxation of the left ventricle. In the course of canine experiments designed to elucidate the hemodynamic events responsible for the aortic component of the second heart sound, high-fidelity left ventricular pressure and dP/dt signals were recorded and accelerations detected on the root of the aorta and epicardium at the cardiac apex. The second heart sound was coincident with maximal negative dP/dt and affected its magnitude to a variable and unpredictable extent. This may account for some of the unexpected variations in magnitude of maximal negative dP/dt that have been described in various disease states and in laboratory experiments where the effects of physiologic and pharmacologic interventions have been studied.     

A case of secundum atrial septal defect combined with aortic stenosis and coronary artery disease showing a single second heart sound

We describe an extremely rare case of secundum atrial septal defect with aortic stenosis and coronary artery disease showing a single second heart sound throughout the respiratory cycle by echocardiogram with simultaneous phonocardiogram. Aortic valve closure corresponded to the single second heart sound. We were unable to detect pulmonary valve closure (PVC) on echocardiogram. Because of the presence of pulmonary hypertension, the pulmonary component of the second heart sound (P2) was presumed to be increased in intensity, and the PVC-P2 interval was thought to be abbreviated. Carotid pulse tracing showed a prolongation of the left ventricular ejection time. We concluded that the single second heart sound was due to both prolongation of left ventricular systole and pulmonary hypertension.     

Hemodynamic studies during intermittent left bundle branch block

A patient with intermittent left bundle branch block and moderate aortic insufficiency, presumably due to rheumatic heart disease, is presented.

At retrograde left heart catheterization, left bundle branch block recurred repeatedly and was always converted to normal conduction and left ventricular hypertrophy by administration of oxygen. Electrocardiograms, intracardiac pressures and indicator-dilution curves for cardiac output were recorded with both types of conduction.

The following hemodynamic alterations consistently accompanied intermittent left bundle branch block:

1. 1. There was a significant fall in the systolic pressures in the left ventricle, central aorta and radial artery, a decreased stroke volume and an increased heart rate. These findings suggest that the force and intensity of left ventricular contraction and, consequently, systolic ejection are significantly decreased with the onset of delayed conduction.

2. 2. A prolonged phase of isometric contraction was the most important alteration in the time relationships of the hemodynamic events of ventricular contraction. This resulted in delay in onset and termination of systolic ejection, with a normal duration of the ejection phase. Isometric relaxation was also prolonged proportionately, but duration of diastole shortened as the cardiac rate increased. Prolonged isometric contraction of the left ventricle is probably responsible for the delayed closure of the aortic valve and paradoxic or fixed splitting of the second heart sound very often seen with left bundle branch block.

     

Hysteresis of left ventricular end ejection pressure-dimension relations after acute pressure loading in the intact canine heart

The left ventricular end systolic pressure-volume relation of the isolated canine heart is linear and independent of the loading conditions. The effects of acute pressure loading on the left ventricular end ejection pressure-length relations were studied in the intact canine heart. The lengths of two wall segments of the left ventricle parallel to the minor axis were measured with pairs of miniature piezoelectric crystals. At two levels of filling pressure, with and without control of heart rate, acute increases in left ventricular afterload were produced for six successive beats by occluding the thoracic aorta. After abrupt release of this occlusion, at left ventricular end diastolic pressure less than 10 mmHg, end ejection lengths were longer than before the occlusion for both segments despite the same or lower end ejection pressures. When heart rate was not controlled the mean(SD) difference in end ejection length was 0.46(0.21) mm (n = 100). When heart rate was controlled by atrial pacing after autonomic blockade the difference was 0.37(0.11) mm (n = 80). In contrast, at left ventricular end diastolic pressure greater than 10 mmHg there was no significant difference between end ejection lengths before and after release of the aortic occlusion. Gradual release of the aortic occlusion over 4-5 beats produced clockwise hysteresis of the left ventricular end ejection pressure-length relation when left ventricular end diastolic pressure was less than 10 mmHg. No hysteresis occurred when left ventricular end diastolic pressure was greater than 10 mmHg. Hysteresis of the end systolic pressure-dimension relation was also seen when major and minor axis dimensions of the left ventricular were measured.(ABSTRACT TRUNCATED AT 250 WORDS)     

血压逆向梯度与重搏波的形成

本文用带二个血压传感器的导管测定了12条狗主动脉的血压波形.二传感器之间相距5厘米,分析了主动脉不同部位血压值的变化.特别是逆向血压梯度的形成,认为动脉血流的惯性及左心室的舒张是重搏波切迹前短时期内近心端血压低于远心端血压的主要原因,在动脉中存在着惯性动能与压力势能之间的相互转化.在此过程中形成了重搏波,而血压波的反射并不是形成重搏波的主要原因.并研究了多巴酚丁胺和硝酸甘油对重搏波的影响.     

Therapeutic significance of controlling heart rate in aortic regurgitation (author's transl)]

The hemodynamic effects of aortic regurgitation are characterized by an increase of left ventricular volume load due to the diastolic regurgitation and a decrease of aortic diastolic pressure or coronary perfusion pressure. It is presumed that an increase of heart rate in such a situation diminishes the regurgitant flow and elevates the coronary perfusion pressure so far as it is not accompanied by an improper increase of myocardial oxygen consumption. The present study, although it was the one performed on dog heart with an aortoventricular shunt rather than aortic valvular destruction, demonstrated that the increase of heart rate, if not beyond 160 beats per min, minimizes regurgitant flow as well as regurgitant ratio and maintains effective cardiac output without impairing coronary circulation. Thus it is suggested that it would be of beneficial therapeutic means in aortic regurgitation to keep the heart rate high or, at least, to avoid its excessive deceleration.