Contractile and relaxation reserve of the left ventricle. III. Patients with cardiomyopathy (author's transl)

Seven of 22 patients with cardiomyopathy increased maximal rate of left ventricular pressure rise (max dP/dt) above 3200 mm Hg/s and dP/dt/P above 60/s. Relaxation reserve was normal with an increase of min dP/dt above 2400 mm Hg/s.--In 15 patients contractile and relaxation reserve was reduced. In congestive cardiomyopathy, contractility and relaxation reserve were equally reduced. Left ventricular enddiastolic pressure increased during exercise slightly or not (grade 1). Enddiastolic volume was elevated to 173 +/- 50 ml/1.73 m2 and endsystolic volume to 63 +/- 22 ml/1.73 m2; ejection fraction and mean circumferential fiber shortening were reduced (61 +/- 17%; 1.3 +/- 0.9 circ/s). In hypertrophic cardiomyopathy without obstruction, contractile and relaxation reserve and ejection phase parameters could be found to be normal. Enddiastolic pressure at rest was elevated. In severe cases, contractile and relaxation reserve were markedly reduced and enddiastolic pressure increased to a greater extent than in congestive cardiomyopathy. In addition, relaxation reserve was reduced, especially in patients with excessive hypertrophy of the myocardium. These had abnormal (grade 2) and pathological reaction to exercise: contractile and relaxation reserve were decreased and enddiastolic pressure (grade 3) increased. Left ventricular contractility was found to be almost normal in patients with hypertrophic obstructive cardiomyopathy. This was the case despite increases in enddiastolic pressure. Contractile reserve was reduced, however, in patients with excessive hypertrophy. Diastolic filling was impeded during exercise.--Measuring left ventricular function during exercise, different types of cardiomyopathy correlate with typical hemodynamic alterations.     

Contractile and relaxation reserve of the left ventricle. IV. Patients with coronary heart disease (author's transl)

51 patients with coronary heart disease had exercise tests on a bicycle ergometer (86 +/- 32 watts). Compared to a normal control group, only 13 patients had normal contractile reserve (group 4.1). In 32 patients the increase in contractility during exercise was reduced (max dP/dt below 3200 mm Hg/s, group 4.2). Patients with reduced contractile reserve were graded according to the height of left ventricular enddiastolic pressure during exercise: In patients with grade 1, enddiastolic pressure was normal. In patients with grade 2, enddiastolic pressure increased between + 4 and + 15 mm Hg and in the patients with grade 3a a above + 15 mm Hg. Contractile and relaxation reserve decreased along with a rise in enddiastolic pressure and an increase in the complaints of the patients. Severe chest pain led to termination of exercise in patients of grade 3b. Enddiastolic pressure increased above + 15 mm Hg. During ischemia, peak-measured velocity of contractile elements (dP/dt/P) and the maximal rate of left ventricular pressure fall (min dP/dt) decreased. In conclusion, with increasing chest pain a decrease of contractile reserve was observed. Left ventricular enddiastolic pressure rose excessively. This has to be taken as a sign of myocardial failure due to ischemic dyskinesia and impeded relaxation.     

Prediction of postoperative performance in aortic valve disease

A new direct method has been developed for predicting postoperative performance in patients undergoing aortic valve replacement. Employing micromanometry and cineangiography, a number of conventional hemodynamic and angiographic variables, including the peak value of the first derivative of ventricular pressure divided by ventricular pressure (dP/dt/P)_max were evaluated in 171 patients studied preoperatively and in 44 patients studied pre- and postoperatively with an additional 14 patients serving as control subjects. Normal contractile state relations (dP/dt/P)_max versus end-diastolic pressure (over a range of 15 mm Hg or less to more than 15 mm Hg) were derived from patients whose preoperative ejection fraction and peak wall'stress were equal to or more than control mean — 2 standard deviations. Postoperative function was predicted to be abnormal (ejection fraction less than control mean — 2 standard deviations) if preoperative values of (dP/dt/P)_max and enddiastolic pressure fell below the 95 percent confidence bands of these contractile state relations.The method accurately predicted postoperative function in 40 of 44 patients with a sensitivity of 100 percent. This result was confirmed by a discriminant function analysis (based on preoperative ejection fraction, end-diastolic pressure and [dP/dt/P]_max) that yielded correct classifications in 42 of 44 patients. These studies indicate that the preoperative contractile state of the myocardium is the major determinant of postoperative performance in aortic valve disease.     

Effects of verapamil and nifedipine on rate of left ventricular relaxation in coronary arterial disease patients

We have evaluated the effects of nifedipine and verapamil on rate of left ventricular relaxation in 26 patients having coronary arterial disease with normal ejection fraction and normal left ventricular contractility. None of the patients had myocardial infarction. All patients showed normal contractile indices and abnormally high values of T constant, neg, dP/dt and left ventricular protodiastolic pressure, suggesting an impairment of left ventricular relaxation. Nifedipine, injected intravenously (15 micrograms/kg) in 14 patients induced a significant reduction of afterload parameters and an increase of contractility. Nifedipine also improved left ventricular relaxation, as it induced a reduction of the T constant from 42 +/- 2 msec to 33 +/- 2 msec (P less than 0.01). It induced a tendency to a reduction of negative dP/dt and protodiastolic pressure without reaching statistical significance. Verapamil, injected intravenously in the remaining 12 patients (0.1 mg/kg as a bolus followed by chronic infusion of 0.005 mg/kg/min for 3 min) induced a reduction of the T constant from 43 +/- 10 to 37 +/- 6 msec (P less than 0.01). It reduced the negativity of dP/dt from 2302 +/- 273 to 2021 +/- 252 mm Hg/sec (P less than 0.05) and of left ventricular protodiastolic pressure from 3.2 +/- 1.4 to 1.5 +/- 1.1 mm Hg (P less than 0.01). Verapamil, like nifedipine, reduced the afterload parameters although to a lesser extent. It did not substantially affect the left ventricular contractility. These data suggest that abnormalities of left ventricular relaxation may precede changes in systolic function and that nifedipine and verapamil favourably modify the indices of left ventricular diastolic function in patients with coronary arterial disease.     

Improvement of left ventricular function after percutaneous transluminal coronary angioplasty

Cardiac function and left ventricular dynamics were measured in seven consecutive patients 1 day before and 6 months after percutaneous transluminal balloon angioplasty of subtotal proximal stenosis of the left anterior descending coronary artery. Before angioplasty all patients had obvious left ventricular dysfunction during exercise and to a smaller degree during isoproterenol infusion; the condition of all patients was greatly improved 6 months after angioplasty. After angioplasty, left ventricular end-diastolic pressure was normal at rest and decreased from a mean (± standard error of the mean) of 33.8 ± 1.6 to 19.2 ± 0.5 mm Hg on exercise. Left ventricular ejection fraction, measured by a gated blood pooling technique with technetium-99m, improved on exercise from 46 ± 5.0 percent to 69 ± 1.0 percent. Cardiac output and stroke volume index increased significantly with exercise after angioplasty. The peak negative rate of pressure reduction in the left ventricle (dP/dt/min), an index of left ventricular relaxation, was highly abnormal on exercise before (2,307 ± 260 mm Hg/s) and increased to the normal range (3,154 ± 200 mm Hg/s) after angioplasty. The improvement in left ventricular function after transluminal angioplasty in these cases of proximal left anterior descending coronary arterial stenosis is extremely encouraging.     

Right ventricular contractile function in children with congenital heart disease

Indexes of right ventricular (RV) systolic function were evaluated in 41 patients undergoing cardiac catheterization. High-fidelity tracings were used to determine RV pressure, maximal RV dP/dt and the velocity of contractile element shortening at a developed pressure of 10 mm Hg (VCE10). In 14 children with an RV systolic pressure less than 35 mm Hg, normal RV volume, pulmonary vascular resistance (PVR) less than 3 units X m2 and no shunts (our normal group), mean (+/- standard deviation) RV dP/dt was 437 +/- 116 mm Hg X s-1 and VCE10 was 1.15 +/- 0.33 muscle length X s-1. In patients with RV systolic hypertension due to valvular pulmonary stenosis or isolated increases in PVR, mean values for RV dP/dt and VCE10 were significantly (p less than 0.05) greater than the normal values. In patients with a ventricular septal defect, RV hypertension and normal PVR, VCE10 was normal but RV dP/dt was significantly elevated. Children with chronic RV volume overload had normal RV contractile indexes. No patient in any group had values for RV dP/dt or VCE10 that were less than normal (mean normal - 2 standard deviations). This study establishes for the first time the indexes of RV isovolumic systole in children. It also shows that RV contractile function is preserved in young patients with chronic RV pressure or volume overload who do not have overt congestive heart failure.     

Effects of abnormal activation on the time course of the left ventricular pressure pulse in dilated cardiomyopathy.

OBJECTIVE--To investigate the effects of QRS duration on characteristics of the left ventricular pressure pulse derived from the time course of functional mitral regurgitation by continuous wave Doppler. DESIGN--Retrospective and prospective study of 50 patients with dilated cardiomyopathy, by electrocardiography, echocardiography, and Doppler cardiography. SETTING--Tertiary cardiac referral centre. PATIENTS--50 patients (mean age (SD) 58 (16)) with dilated cardiomyopathy, all with functional mitral regurgitation. RESULTS--The values of QRS duration ranged widely, from 70 to 190 ms with a mean value of 110 ms, and were unimodally distributed. The overall duration of mitral regurgitation correlated positively with QRS time (r = 0.65) over the entire range of values. When the duration of mitral regurgitation was divided into contraction, aortic ejection, and relaxation times, increased QRS duration prolonged contraction (r = 0.51) and relaxation (r = 0.52) times. Aortic ejection time was affected by RR interval (r = 0.74). Duration of QRS correlated negatively with peak rate of rise in left ventricular pressure (+dP/dt) (r = -0.48), and positively with the time intervals from Q to peak pressure (r = 0.49) and to peak +dP/dt (r = 0.72), and also with those from the start of mitral regurgitation to peak pressure (r = 0.49) and to peak +dP/dt (r = 0.76). Duration of QRS did not directly affect the peak rate of left ventricular pressure fall (-dP/dt), or the isovolumic relaxation period. CONCLUSIONS--Values of QRS duration are unimodally distributed in patients with dilated cardiomyopathy, without evidence of a discrete group of patients with left bundle branch block. Prolonged QRS duration reduces peak +dP/dt, prolongs overall duration of the pressure pulse, the time to peak +dP/dt, and relaxation time. Duration of QRS must therefore be taken into account in assessing standard measurements of myocardial function in patients with dilated cardiomyopathy.     

Effect of increasing heart rate on left ventricular performance in patients with normal cardiac function

The influence of an increase in heart rate on left ventricular (LV) contractile performance was assessed in patients with normal LV function. In 19 patients (3 men, 16 women) ages 55 +/- 9 years (mean +/- standard deviation) with normal global and segmental LV function and normal coronary arteries, LV dP/dt max was measured at baseline heart rate and during atrial pacing at baseline +5, baseline +25 and baseline +45 beats/min. In 10 of the patients, intravascular volume was not altered during pacing and, as a result, echocardiographically measured LV end-diastolic dimension decreased (5.4 +/- 0.4 at baseline vs 4.9 +/- 0.5 cm at baseline +45 beats/min, p less than 0.05). In these patients, LV dP/dt max increased modestly (1,571 +/- 237 at baseline vs 1,760 +/- 199 mm Hg/s at baseline +45 beats/min, p less than 0.05). In the other 9 patients, intravascular volume was expanded rapidly (by saline infusion) during pacing and, as a result, LV end-diastolic dimension was held constant (5.2 +/- 0.6 at baseline vs 5.1 +/- 0.6 cm at baseline +45 beats/min, difference not significant). In these patients, LV dP/dt max increased substantially with pacing (1,505 +/- 228 at baseline vs 2,050 +/- 258 mm Hg/s at baseline +45 beats/min, p less than 0.05). Thus, an increase in heart rate induces a modest increase in LV dP/dt max in patients in whom LV preload (as reflected by end-diastolic dimension) is allowed to decrease; in contrast, it causes a marked increase in LV dP/dt max in those in whom LV preload is maintained constant.     

Hemodynamic and volume correlates of left ventricular diastolic relaxation and filling in patients with aortic stenosis.

OBJECTIVE. The aim of the present study was to evaluate the hemodynamic and volume correlates of early diastolic filling and isovolumetric relaxation in patients with aortic stenosis. BACKGROUND. Left ventricular diastolic relaxation and filling have been found to be heterogeneous in patients with aortic stenosis. Potential mechanisms underlying this heterogeneity include individual differences in the severity of muscle hypertrophy or systolic dysfunction, or both, in the presence and severity of mitral regurgitation and in the level of left atrial pressure. METHODS. Right (fluid-filled) and left (high fidelity micromanometer) ventricular pressures, left ventricular volumes (contrast angiography) and transmitral inflow dynamics (Doppler echocardiography) were measured in 17 patients with isolated severe aortic stenosis (valve area less than 0.75 cm2). Measurements included left ventricular end-diastolic and end-systolic volumes, left ventricular ejection fraction, peak positive and negative first derivative of left ventricular pressure (dP/dt), the time constant of isovolumetric relaxation (tau), left ventricular end-diastolic pressure, left ventricular mass, left ventricular end-systolic stress, mean capillary wedge pressure and peak early (E) and late (A) transmitral filling velocities. Patients were subclassified according to left ventricular ejection performance at rest and mean capillary wedge pressure. RESULTS. Patients with normal ejection performance and normal mean capillary wedge pressure had a normal rate of isovolumetric left ventricular pressure decay and an abnormal diastolic filling pattern, with diastolic filling occurring primarily during atrial systole. In contrast, in patients with systolic dysfunction and elevated mean capillary wedge pressure, isovolumetric pressure decay was prolonged and diastolic filling occurred essentially during the rapid filling period, with reduced atrial contribution to left ventricular filling and a short isovolumetric relaxation period. Stepwise multiple linear regression analysis identified two variables as independent predictors of transmitral velocity profile and three variables independently predictive of the rate of left ventricular pressure decay. The single most important predictor of transmitral filling pattern was the pulmonary capillary wedge pressure (p less than 0.0001), followed by the left ventricular peak negative dP/dt (p = 0.002). The single most powerful predictor of the rate of reduction in left ventricular pressure was left ventricular mass index (p less than 0.0001), followed by end-systolic volume index (p = 0.0002) and left ventricular peak negative dP/dt (p = 0.0029). CONCLUSIONS. In patients with aortic stenosis, left ventricular filling is essentially determined by left atrial pressure, whereas isovolumetric relaxation more closely depends on the severity of muscle hypertrophy and chamber dilation.     

Noninvasive estimation of the instantaneous first derivative of left ventricular pressure using continuous-wave Doppler echocardiography

BACKGROUND. The complete continuous-wave Doppler mitral regurgitant velocity curve should allow reconstruction of the ventriculoatrial (VA) pressure gradient from mitral valve closure to opening, including left ventricular (LV) isovolumic contraction, ejection, and isovolumic relaxation. Assuming that the left atrial pressure fluctuation is relatively minor in comparison with the corresponding LV pressure changes during systole, the first derivative of the Doppler-derived VA pressure gradient curve (Doppler dP/dt) might be used to estimate the LV dP/dt curve, previously measurable only at catheterization (catheter dP/dt). METHODS AND RESULTS. This hypothesis was examined in an in vivo mitral regurgitant model during 30 hemodynamic stages in eight dogs. Contractility and relaxation were altered by inotropic stimulation and hypothermia. The Doppler mitral regurgitant velocity spectrum was recorded along with simultaneously acquired micromanometer LV and left atrial pressures. The regurgitant velocity profiles were digitized and converted to VA pressure gradient curves using the simplified Bernoulli equation. The instantaneous dP/dt of the VA pressure gradient curve was then derived. The instantaneous Doppler-derived VA pressure gradients, instantaneous Doppler dP/dt, dP/dtmax, and -dP/dtmax were compared with corresponding catheter measurements. This method of estimating dP/dtmax from the instantaneous dP/dt curve was also compared with a previously proposed Doppler method of estimating dP/dtmax using the Doppler-derived mean rate of LV pressure rise over the time period between velocities of 1 and 3 m/sec on the ascending slope of the Doppler velocity spectrum. Both instantaneous Doppler-derived VA pressure gradients (r = 0.95, p less than 0.0001) and Doppler dP/dt (r = 0.92, p less than 0.0001) correlated well with corresponding measurements by catheter during systolic contraction and isovolumic relaxation (pooled data). The Doppler dP/dtmax (1,266 +/- 701 mm Hg/sec) also correlated well (r = 0.94) with the catheter dP/dtmax (1,200 +/- 573 mm Hg/sec). There was no difference between the two methods for measurement of dP/dtmax (p = NS). Although Doppler -dP/dtmax was slightly lower than the catheter measurement (961 +/- 511 versus 1,057 +/- 540 mm Hg/sec, p less than 0.01), the correlation between measurements by Doppler and catheter was excellent (r = 0.93, p less than 0.0001). The alternative method of mean isovolumic pressure rise (896 +/- 465 mm Hg/sec) underestimated the catheter dP/dtmax (1,200 +/- 573 mm Hg/sec) significantly (on average, 25%; p less than 0.001). CONCLUSIONS. The present study demonstrated an accurate and reliable noninvasive Doppler method for estimating instantaneous LV dP/dt, dP/dtmax, and -dP/dtmax.     

Acute effects of cardiac resynchronization therapy on functional mitral regurgitation in advanced systolic heart failure

OBJECTIVES: We studied the acute effects of cardiac resynchronization therapy (CRT) on functional mitral regurgitation in heart failure (HF) patients with left bundle branch block (LBBB). BACKGROUND: Both an decrease [corrected] in left ventricular (LV) closing force and mitral valve tethering have been implicated as mechanisms for functional mitral regurgitation (FMR) in dilated hearts. We hypothesized that an increase in LV closing force achieved by CRT could act to reduce FMR. METHODS: Twenty-four HF patients with LBBB and FMR were studied after implantation of a biventricular CRT system. Acute changes in FMR severity between intrinsic conduction (OFF) and CRT were quantified according to the proximal isovelocity surface area method by measuring the effective regurgitant orifice area (EROA). Results were compared with the changes in estimated maximal rate of left ventricular systolic pressure rise (LV+dP/dt(max)) and transmitral pressure gradients (TMP), both measured by Doppler echocardiography. RESULTS: Cardiac resynchronization therapy was associated with a significant reduction in FMR severity. Effective regurgitant orifice area decreased from 25 +/- 19 mm(2) (OFF) to 13 +/- 8 mm(2) (CRT). The change in EROA was directly related to the increase in LV+dP/dt(max) (r = -0.83, p < 0.0001). Compared with OFF, TMP increased more rapidly during CRT, and a higher maximal TMP was observed (OFF 73 +/- 24 mm Hg vs. CRT 85 +/- 26 mm Hg, p < 0.01). CONCLUSIONS: Functional mitral regurgitation is reduced by CRT in patients with HF and LBBB. This effect is directly related to the increased closing force (LV+dP/dt(max)). The results support the hypothesis that an increase in TMP, mediated by a rise in LV+dP/dt(max) due to more coordinated LV contraction, may facilitate effective mitral valve closure.     

Impaired maximal rate of left ventricular relaxation in patients with coronary artery disease and left ventricular dysfunction.

It has been suggested that the rate of left ventricular (LV) relaxation is related to the inotropic state, end-systolic fiber length and peak LV pressure, but little information is available regarding the rate of LV relaxation in patients with coronary artery disease (CAD) and LV dysfunction. To assess the rate of LV relaxation we obtained high-fidelity LV pressure measurements with manometer-tip catheters in 39 patients. The signal was analyzed by a digital computer to yield the maximal rate of pressure rise (pos dP/dt) and the maximal rate of pressure fall (neg dP/dt). Selective coronary arteriography and biplane LV angiography with determination of LV volumes, ejection fraction (EF) and percent abnormally contracting segments (ACS) when present, were performed in all patients. In 10 patients with normal LV function (EF greater than 0.50, no asynergy) mean neg dP/dt (2074 +/- 121 mm Hg/sec) was significantly (p less than 0.01) greater than in 29 patients with CAD and LV dysfunction (1695 +/- 66 mm Hg/sec). In nine patients with LV dysfunction and EF less than 0.35, mean neg dP/dt was reduced to 1405 +/- 107 mm Hg/sec, significantly (p less than 0.01) lower than in patients with normal LV function. Neg dP/dt correlated well with pos dP/dt (r = 0.75), with EF (r = 0.74), and with ACS (r = -0.74), and less well with LV end-systolic volume (r = 0.67). There was very poor correlation between neg dP/dt and peak LV pressure (r = 0.30). These data suggest that the rate of LV relaxation, as assessed by neg dP/dt, is impaired in patients with CAD and LV dysfunction, and the extent of impairment is related to the severity of the dysfunction as determined hemodynamically by pos dP/dt, and angiographically by EF and ACS. In these patients the maximal rate of LV relaxation is inversely related to LV end-systolic volume, and is not related to peak LV pressure.     

Effects of nifedipine on diastolic function during brief periods of flow-limiting ischemia in the conscious dog

To determine the contribution of transsarcolemmal calcium flux to abnormal diastolic function produced by brief periods of flow-limiting ischemia and reperfusion, we evaluated early and late diastolic function during transient coronary occlusion and reperfusion before and during administration of intravenous nifedipine (NIF) (10 +/- 1 microgram/kg/min) in nine preinstrumented conscious dogs. We also assessed the effects of nitroprusside (NTP) (2 +/- 0.2 micrograms/kg/min) during an identical period of ischemia and reperfusion to independently assess the consequences of altered loading alone on diastolic function. To minimize the effects of temporal dysynchrony and altered ventricular loading conditions on isovolumetric relaxation, we developed a conscious dog preparation of reversible transient (30 to 60 sec) bilateral coronary occlusion (BCO). BCO was characterized by significant systolic depression: maximum (+)dP/dt decreased (from 2617 +/- 600 to 1981 +/- 565 mm Hg/sec, p less than .05), left ventricular transverse dimension shortening diminished (from 20 +/- 5 to 9 +/- 5%, p less than .05), and the left ventricle dilated (42.4 +/- 6.4 to 43.8 +/- 6.3 mm, p less than .05). Concomitantly the time constants of isovolumetric relaxation prolonged (from 22 +/- 3 to 28 +/- 4 msec, p less than .05) and minimal diastolic left ventricular pressure increased (from -3 +/- 6 to 6 +/-6 mm Hg, p less than .05). The passive diastolic pressure-dimension relationship shifted upward and to the right and was associated with increased chamber stiffness (from 0.50 +/- 0.26 to 1.03 +/- 0.53 mm Hg/mm, p less than .05) and increased left ventricular end-diastolic pressure (from 7 +/- 7 to 19 +/- 7 mm Hg, p less than .05). Reperfusion immediately after BCO was characterized by prompt restoration of systolic contractile performance [maximum (+)dP/dt 3220 +/- 530 mm Hg/sec] but persistently abnormal early and late diastolic function (time constant of isovolumetric relaxation 30 +/- 6 msec, left ventricular end-diastolic pressure 20 +/- 7 mm Hg). The effects of drug administration on ventricular function during BCO were then evaluated under matched loading conditions. NTP improved time constant of isovolumetric relaxation (20 +/- 8 vs 28 +/- 4 msec, p less than .05) and minimal diastolic left ventricular pressure (2 +/- 5 vs 6 +/- mm Hg, p less than .05) during BCO, but NIF did not (time constant of isovolumetric relaxation 27 +/- 6 msec, minimal diastolic left ventricular pressure 7 +/- 5 mm Hg).(ABSTRACT TRUNCATED AT 400 WORDS)     

Alterations in left ventricular relaxation during atrioventricular pacing in humans

To determine whether the asynchronous left ventricular contraction-relaxation sequence that exists during right ventricular pacing alters left ventricular relaxation, measurements of both the maximal rate of decline of left ventricular pressure (peak negative dP/dt) and the time constant of left ventricular relaxation were obtained during atrial and atrioventricular (AV) pacing in 25 patients referred for diagnostic cardiac catheterization. Heart rate was maintained at 10 to 15 beats/min above the sinus rate at rest, and relaxation was assessed during atrial pacing, AV pacing and repeat atrial pacing. The patients were classified into two groups. Group 1 included 10 patients with normal left ventricular systolic function at rest (ejection fraction greater than 0.55) and without evidence of prior myocardial infarction. Group 2 included 15 patients with a depressed left ventricular ejection fraction or akinesia of one or more left ventricular segments on the contrast ventriculogram, or both. Heart rate, peak left ventricular systolic pressure, end-systolic pressure and end-diastolic pressure remained constant during atrial, AV pacing and repeat atrial pacing in all patients. In group 1 patients, the decrease in peak negative dP/dt (1,507 +/- 200 versus 1,424 +/- 187 mm Hg/s) and the increase in the time constant of left ventricular relaxation (48 +/- 11 versus 51 +/- 11 ms) during AV pacing was not significantly different when compared with values during atrial pacing.(ABSTRACT TRUNCATED AT 250 WORDS)     

Treadmill exercise test in aortic stenosis and mitral stenosis.

The incidence of positive submaximal treadmill exercise tests was evaluated in patients with mitral stenosis and aortic stenosis, no electrocardiographic evidence of left ventricular hypertrophy, and normal coronary arteries on angiography. Seven of 19 patients (37 percent) with aortic stenosis (53 to 80 mm Hg gradient across the aortic valve) had greater than or equal to 1.0 mm of ischemic S-T segment depression during or after a submaximal treadmill test. Three of 15 patients (20 percent) with mitral stenosis (11 to 22 mm Hg mean gradient across the mitral valve) had greater than or equal to 1.0 mm of ischemic S-T segment depression during or after a submaximal treadmill exercise test. Patients with significant valvular disease, no electrocardiographic evidence of left ventricular hypertrophy, and normal coronary arteries may have a positive submaximal treadmill exercise test due to an unfavorable balance between myocardial oxygen supply and myocardial oxygen demand.     

Load independence of the rate of isovolumic relaxation in man

This investigation was designed to determine whether the rate of isovolumic left ventricular pressure decline is affected by load in man. Fourteen patients were instrumented with micromanometer left ventricular and right atrial pacing catheters to maintain a constant heart rate during control conditions and infusion of methoxamine or nitroprusside. The isovolumic relaxation period was defined as the time from peak (-)dP/dt to 5 mm Hg above left ventricular end-diastolic pressure of the following beat. The rate of isovolumic relaxation was calculated as time constants (Tau) from the linear regression of natural log pressure vs time (Tln) and instantaneous (-)dP/dt vs pressure (TD), which includes a variable asymptote (PB). The mean heart rates and average (+)dP/dt values normalized at 40 mm Hg development pressure (DP40) did not differ significantly, despite 33% and 43% increases in left ventricular peak and end-diastolic pressures during the infusion of methoxamine (p less than .001 and p less than .01, respectively) and 24% and 29% decreases during the infusion of nitroprusside (p less than .001 and p less than .01, respectively). The average Tln and TD values were not significantly affected by these alterations in load. In two patients, an inverse linear relationship was demonstrated between decreases in Tau and increases in contractile state produced by an infusion of dobutamine, as shown by correlation of Tln and TD with (+)dP/dt/DP40 (r = -.88 and -.83, respectively). We conclude that the time constants of left ventricular isovolumic relaxation are unaffected by modest alterations in loading conditions in man when heart rate is maintained constant.(ABSTRACT TRUNCATED AT 250 WORDS)     

Monophasic transmitral flow pattern with less increase in heart rate indicates left ventricular dysfunction.

When heart rate (HR) increases, mitral flow can become monophasic. Prolonged isovolumic contraction and relaxation time (ICT and IRT), directly related to left ventricular (LV) function, can potentially influence the HR with monophasic mitral flow. The present study investigated the relation between HR that causes monophasic flow and LV function. During diagnostic catheterization, HR was increased using right atrial pacing by 2 beats/min every 2 min in a stepwise manner until the development of monophasic mitral flow in 17 patients with normal sinus rhythm. ICT, IRT, end-diastolic and end-systolic LV volumes, LV ejection fraction, LV peak + and -dP/dt, peak (+dP/dt)/P, and the relaxation time constant (tau) were measured by Doppler echocardiography or catheterization when monophasic mitral flow developed. The monophasic HR varied from 74 to 106 beats/min. By univariate analysis, ICT (p<0.01, r2=0.73), LV peak +dP/dt (p<0.05, r2=0.37), peak (+dP/dt)/P (p<0.01, r2=0.71), peak -dP/dt (p<0.05, r2=0.25), and tau (p<0.05, r2=0.33) had a significant correlation with monophasic HR. By multivariate analysis, prolonged ICT and reduced LV peak -dP/dt independently contributed to monophasic mitral flow with less increase in HR. Monophasic mitral flow with less increase in HR indicates impaired LV systolic and diastolic function during isovolumic contraction and relaxation.     

Diastolic unloading and improved LV pump efficiency early after repair of the insufficient mitral valve

BACKGROUND: This study aimed to evaluate the acute effect of mitral valve repair (MVR) on LV hemodynamics and geometry in patients with normal ventricular function. METHODS: In 10 patients with severe mitral regurgitation undergoing MVR, pressure-volume relationships were recorded before annuloplasty prior to and after hemodilution and after MVR during stable circulatory condition, using the conductance catheter technique (CC). Analyses were done off-line; volume calibration was based on data obtained after completion of valve repair (mean +/- s.d.). RESULTS: CC showed that only 61 +/- 15 % of left ventricular output was ejected into the systemic circulation, regurgitation volume being 39 +/- 15 %. MVR led to a reduction in LV stroke work index from 4.7 +/- 1.8 mm Hg x l x m (-2) at before valve repair to 2.2 +/- 1.0 mm Hg x l x m (-2) after surgery at unchanged cardiac index. LV diastolic filling parameters improved: LV relaxation time constant tau decreased from 52 +/- 15 to 37 +/- 11 ms and dP/dt (min) increased from - 873 +/- 231 to - 1286 +/- 283 mm Hg x s (-1). CONCLUSIONS: Despite cardioplegic arrest, MVR leads to acute improvement of diastolic LV function early after the operation. This may explain why valve repair has an acute positive effect in patients with impaired LV function.     

Continuous wave Doppler echocardiography for noninvasive assessment of left ventricular dP/dt and relaxation time constant from mitral regurgitant spectra in patients

Objectives. We previously demonstrated experimentally that the mitral regurgitant velocity spectrum can be used to estimate left ventricular pressure throughout systole and may provide a new noninvasive method for estimating maximal dP/dt and the relaxation time constant. This study was designed to test this method in patients.Background. The maximal first derivative of left ventricular pressure (dP/dt) and the time constant of left ventricular isovolumetric relaxation (τ) are important variables of left ventricular function, but the need for invasive measurement with high fidelity catheters has limited their use in clinical cardiology.Methods. Twelve patients with mitral regurgitation were studied. The Doppler mitral regurgitant velocity spectrum was recorded simultaneously with micromanometer left ventricular pressure tracings in all patients. The regurgitant velocity profiles were digitized and converted to ventriculoatrial (VA) pressure gradient curves using the simplified Bernoulli equation and differentiated into instantaneous dP/dt. The relaxation time constant (τ) was calculated assuming a zero pressure asymptote from catheter left ventricular pressure decay (τ_c) and forn the Dopplerderived VA gradient curve with corrections. Two methods were used to correct the Doppler gradient curve to better approximate the left ventricular pressure decay before calculating the relaxation time constant: 1) adding an arbitrary 10 mm Hg (τ₁₀), and 2) adding the actual mean pulmonary capillary pressure (τ_la).Results. The Doppler-derived maximal positive dP/dt (1,394 ± 302 mm Hg/s [mean ± SD]) correlated well (r = 0.91) with the catheter-derived maximal dP/dt (1,449 ± 307 mm Hg/s). Although the Doppler-derived negative maximal dP/dt differed slightly from catheter measurement (1,014 ± 289 vs. 1,195 ± 354 mm Hg/s, p < 0.01), the correlation between Doppler and catheter measurements was similarly good (r = 0.89, p < 0.0001). The correlation between τ₁₀and τ_cwas excellent (r = 0.93, p < 0.01), but the Doppler-derived τ₁₀(50.0 ± 11.0 ms) slightly underestimated the catheter-derived τ_c(55.5 ± 12.8 ms, p < 0.01). This slight underestimation could be corrected by adding the actual pulmonary capillary wedge pressure to the Doppler gradient curve.Conclusions. Doppler echocardiography provides an accurate and reliable method for estimating left ventricular maximal positive dP/dt, maximal negative dP/dt and the relaxation time constant (τ) in patients with mitral regurgitation.     

Relation between exercise capacity and left ventricular systolic versus diastolic function during exercise in patients after myocardial infarction

BACKGROUND: It is known that left ventricular systolic function at rest does not correlate well with exercise capacity of patients with heart failure. However, the contribution of left ventricular diastolic dysfunction, especially during exercise, to exercise capacity of cardiac patients remains to be determined. OBJECTIVE: To determine the impact of left ventricular systolic and diastolic function during exercise on exercise capacity of patients with left ventricular dysfunction after myocardial infarction. METHODS: A symptom-limited exercise test was performed with measurements for hemodynamics and uptake of oxygen (Vo2) of 26 men who had previously suffered myocardial infarction. These patients were divided into two groups according to their peak Vo2 (group 1 with peak Vo2 > or = 16 ml/kg per min, n= 13; and group 2 with peak Vo2 < 16 ml/kg per min, n= 13). Pulmonary arterial pressure, left ventricular and systemic arterial pressure, and cardiac output were measured at rest and during exercise. RESULTS: At rest, there was no difference between the two groups in terms of hemodynamic parameters except for minimal dP/dt, minimal left ventricular pressure (LVP) and time constant for decay of left ventricular pressure (tau). During peak exercise, cardiac output, left ventricular end-diastolic pressure (EDP), minimal dP/dt, minimal LVP, and tau for the two groups were significantly different. Furthermore, peak Vo2 was significantly correlated with T, minimal LVP, minimal dP/dt, EDP, and maximal dP/dt during peak exercise for the whole group of patients. CONCLUSION: Left ventricular diastolic function during exercise, i.e. diastolic reserve, may be an important determinant of exercise capacity of patients with left ventricular dysfunction after myocardial infarction.