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Purpose: We sought to determine the importance of a third heart sound (S(3)) and its relation to hemodynamic and valvular dysfunction., Subjects and Methods: We prospectively enrolled 580 patients who had isolated valvular regurgitation (mitral, n = 299; aortic, n = 121) or primary left ventricular dysfunction with or without functional mitral regurgitation (n = 160). We analyzed the associations between the clinical finding of an audible S(3) (as noted in routine clinical practice by internal medicine physicians) and hemodynamic alterations measured by comprehensive quantitative Doppler echocardiography., Results: S(3) was more prevalent in patients with primary left ventricular dysfunction (46%, n = 73) than in organic mitral (16%, n = 47) or aortic (12%, n = 14) regurgitation (P <0.001). Patients with an S(3) were more likely to have class III-IV symptoms (55% [74 of 137] vs. 18% [80 of 443] of those without an S(3), P <0.001) and had a higher mean [+/- SD] pulmonary pressure (55 +/- 15 vs. 41 +/- 11 mm Hg, P <0.001). An S(3) was also related to a higher early filling velocity due to a greater filling volume, restrictive filling, or both. An S(3) was a marker of severe regurgitation (regurgitant fraction > or =40%) in patients with primary left ventricular dysfunction (odds ratio [OR] = 2.4; 95% confidence interval [CI]: 1.1 to 5.5), mitral regurgitation (OR = 17; 95% CI: 5.8 to 52), and aortic regurgitation (OR = 7.1; 95% CI: 1.8-28). An S(3) was also associated with restrictive filling in primary left ventricular dysfunction (OR = 3.0; 95% CI, 1.6 to 5.9), marked dilatation in mitral regurgitation (OR = 20; 95% CI: 6.8 to 58), and an ejection fraction (<50%) in aortic regurgitation (OR = 19; 95% CI: 6.0 to 62)., Conclusion: An audible S(3) is an important clinical finding, indicating severe hemodynamic alterations, and should lead to a comprehensive assessment and consideration of vigorous medical or surgical treatment.

Likelihood ratio measures may be used as a standard for expressing the predictive power of noninvasive cardiovascular tests, calculated from sensitivity and specificity measures or as ratios of the predictive value odds to pretest odds for positive and negative test results. The positive likelihood ratio, (+)LR, expresses the power of a positive test result to augment an estimate of disease probability independent of the pretest prevalence of disease in a given population; the negative likelihood ratio, (-)LR, expresses the power of a negative test result to augment an estimate of the probability of no disease independent of the pretest prevalence of no disease in the same population. The likelihood ratio principle is applicable to the evaluation of the predictive power of single or combined test results reported for either dichotomous or continuous end points. This part of the perspective exemplifies application of the likelihood ratio principle in a wide variety of testing conditions for coronary artery disease followed by a discussion of the limitations of likelihood ratio computation in test power evaluation. Likelihood ratios provide a more concise and unambiguous standard for calibrating the predictive power of single and combined noninvasive cardiovascular test results than are provided by measures of sensitivity, specificity, and predictive value.

The current practice of reporting positive and negative predictive value (PV), sensitivity (Se), and specificity (Sp) as measures of the power of noninvasive cardiovascular tests has significant limitations. A test result's PV and its comparison with other test results are highly dependent on the pretest disease prevalence at which it is determined; the citation of sensitivity and specificity provides no succinct or explicit quantitation of the rule-in and rule-out power of a test. This article presents a rationale for the use of an alternative standard for expressing predictive power in the form of positive and negative likelihood ratios, (+)LR and (-)LR. The likelihood ratios are composite expressions of test power, which incorporate the Se and Sp and their respective complements [(1 - Se) and (1 - Sp)], thus yielding single unambiguous measures of positive and negative predictive power. The likelihood ratios are calculated as follows: (+)LR = Se/(1 - Sp) and (-)LR = Sp/(1 - Se). On analysis of the predictive value equations, the likelihood ratios equal the quotients of the posttest predictive value odds to the pretest prevalence odds for disease and no disease, respectively, as follows: (+)LR = (+)PVOd/POD and (-)LR = (-)PVOn/PON, where (+)PVOd is positive predictive value odds for disease, POD is prevalence odds for disease, (-)PVOn is negative predictive value odds for no disease, and PON is prevalence odds for no disease. Thus, the likelihood ratios are measures of the odds advantage in posttest probability of disease or no disease relative to pretest probability, independent of disease prevalence in the tested population. The quotients of the (+)LR or the (-)LR among test results studied in a common population are direct expressions of their relative predictive power in that population. The likelihood ratio principle is applicable to the evaluation of the predictive power of multiple tests performed in a common population and to estimating predictive power at multiple test thresholds.

We present an unusual case of hypertrophic cardiomyopathy complicated by mitral regurgitation resulting from chordal rupture with flail posterior mitral leaflet. The diagnosis was suggested by the presence of an anteriorly directed mitral regurgitation jet on transthoracic color flow imaging, in addition to the typical posterolateral-lateral jet caused by systolic anterior mitral motion. The flail posterior leaflet was confirmed by transesophageal echocardiography, and the patient underwent mitral valve repair in addition to myectomy. This combination of hypertrophic cardiomyopathy and flail mitral leaflet usually requires surgical intervention, and prompt diagnosis is important. The presence of an anteriorly directed mitral regurgitant jet should always raise suspicion of posterior mitral leaflet abnormality.

The purpose of this study was to determine if quantitative measurements of regional asynergy add independent prognostic information to global ejection fraction in patients with chronic coronary artery disease. Four hundred eighty-six patients with a history of Q-wave myocardial infarction who underwent gated-equilibrium radionuclide angiography at least 3 months after infarction were monitored for a median duration of 4.7 years. During follow-up there were 95 deaths. Four of five regional asynergy indexes analyzed were associated with overall mortality. The strength of the association between overall mortality and the index that proved to be optimal (univariate chi2 = 26.4, p < 0.001) was stronger than for global ejection fraction (univariate chi2 = 21.5, p < 0.001). For patients with global ejection fraction <40%, 4-year survival was 87% for those with a low asynergy index versus 65% for those with a high asynergy index (p = 0.016). In conclusion, indexes of regional asynergy add independent prognostic information to global left ventricular ejection fraction.

Employing equilibrium-gated radionuclide ventriculography in the left anterior oblique view, six geometric models and five mathematic coefficients of nonuniformity in regional left ventricular emptying were tested for their relative mortality risk-stratifying power and capacity to augment the risk-discriminating potency of the continuous and dichotomized global ejection fraction. Radionuclide ventriculography was performed an average of 7.6 days after acute myocardial infarction. All geometric models significantly separated 20 normal subjects from 137 patients with recent infarction (p less than 0.001). Cumulative mortality data demonstrated that significant independent univariate dichotomizing potency and augmentation of the mortality risk-discriminating power of the global ejection fraction were provided by models of regional emptying that 1) conformed to coronary artery perfusion areas, 2) encompassed total ventricular counts, 3) expressed variability in regional relative to global ejection fraction, and 4) simulated a pattern of emptying directed toward the center of geometry of the left ventricle. The combination of a four quadrant geometric model with axes drawn 45 degrees above the horizontal and a coefficient of variation calculated as square root of sigma(GEF - REF)2/4 x 100/GEF (where GEF = global ejection fraction and REF = regional ejection fraction) proved to be optimal. This coefficient averaged 12.2% in normal subjects and 32.2% in patients with recent acute myocardial infarction (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Initial electrical forces emanating from interventricular septal depolarization, being directed to the right and anteriorly, normally produce an initial negative deflection or Q wave in leads I, aVL and V6 and an initial positive deflection or R wave in leads V1 and V2. The observations of hypertrophied interventricular septum, an integral part of the left ventricle, in patients with left ventricular hypertrophy would predict an increase in these septal electrical forces similar to the total left ventricular (QRS) forces in these subjects. Contrary to this expectation, several studies document an actual decrease or absence of the normally oriented initial forces in ECGs of patients with the criteria of left ventricular hypertrophy. In order to clarify the nature of this paradox, this study was initiated. Our observations suggest that the normal initial septal forces indeed increase as expected, during the initial four to six years, and subsequently show a progressive decline in patients with left ventricular hypertrophy. Although the precise mechanism for the bimodal change in the septal forces during the period of the constancy of the total QRS forces is not clear, a hypothesis based on the current knowledge is advanced to explain these observations.

This study was designed to determine whether left ventricular performance measured noninvasively from the systolic time intervals could identify patients in whom coronary bypass surgery may improve survival. 71 patients with two- or three-vessel disease undergoing coronary bypass surgery were compared with 78 matched medically treated patients. All patients had recuperated from myocardial infarction by a mean of 17.6 months when systolic time intervals were performed. Surgical and medical patients were classified preoperatively into those with normal and those with abnormal left ventricular performance by preejection period/left ventricular ejection time (PEP/LVET less than or equal to 0.42 and greater than 0.42, respectively). Survival was analyzed by life table and log-rank test. Cumulative 5-year survival in patients with normal left ventricular performance was not statistically different in surgical and medical groups (96 vs. 93%, respectively). In contrast, cumulative survival in patients with abnormal left ventricular performance was significantly greater in the surgical group when compared to the medical group (84 vs. 62, p less than 0.01). Among the patients with abnormal left ventricular function, the mean PEP/LVET and the average vessel disease were not different in the medical and surgical groups. Multivariate analysis of 17 other clinical and laboratory risk variables were not different between these two groups. It is concluded that coronary bypass surgery my improve survival in patients with two- or three-vessel disease and left ventricular dysfunction.

Ten consecutive patients with tissue-proven amyloidosis, seven of whom presented with congestive heart failure, were found to exhibit intense diffuse uptake of technetium-99m-pyrophosphate (Tc-99m-PYP) on cardiac radionuclide imaging. The patients exhibited echocardiographic and systolic time interval abnormalities suggesting combined restrictive and congestive cardiomyopathic changes. On M-mode echocardiograms, there was symmetrically increased thickness of the interventricular septum and left ventricular (LV) posterior wall in diastole (10 of 10), decreased fractional shortening of the LV minor axis diameter in systole (eight of nine), and decreased percent thickening of the LV minor axis diameter in systole (eight of nine) and LV posterior wall (10 of 10) in systole. Three patients demonstrated enlarged LV end-diastolic diameter. All 10 patients had abnormal PEP/LVET and eight had shortened LVETI. When combined with noninvasive tests of LV performance, positive myocardial pyrophosphate (PYP) scanning provides a new and useful adjunct in the diagnosis of amyloid heart disease.

Previous observations of slowing of the heart rate after administration of atropine in doses smaller than 0.4 mg and recent reports of development of rhythm disorders in patients with acute myocardial infarction given atropine prompted us to evaluate systematically the effects of various doses of atropine (0.1 to 0.8 mg) on the response of the sinoatrial (S-A) and atrioventricular (A-V) nodes in healthy volunteers. The response of the S-A node to atropine was characteristically bimodal, slowing at smaller doses and accelerating at larger doses. In contrast, the A-V node showed acceleration of conduction in response to all doses of atropine used. A hypothesis based on current understanding of the electrophysiologic parameters governing impulse formation and impulse conduction is advanced to explain the apparent paradox in the S-A and A-V nodal responses to small doses of atropine. The results suggest the need for caution and continuous rhythm monitoring when giving atropine to patients with acute myocardial infarction.

Cardiac arrhythmias are commonly seen in the everyday practice of medicine by the physician. Although certain arrhythmias may be suspected clinically, precise diagnosis is made by electrocardiographic recording of the abnormal rhythm. Once the arrhythmia has been recorded, the next steps are proper electrocardiographic diagnosis and selection of proper treatment. The specific mode of therapy and the speed with which it is delivered will depend not only on the type of arrhythmia, but also on the hemodynamic consequences of the rhythm abnormality on the patient's cardiovascular system. The purpose of this paper is to discuss the electrocardiographic criteria of common cardiac arrhythmias as well as current concepts regarding therapy.

Simultaneous determinations of systolic time intervals (preejection period index [PEPI], left ventricular ejection time index [LVETI] and ratio of preejection period to left ventricular ejection time [PEP/LVET]) and echographic measures of left ventricular performance (percent change in minor axis diameter [%delta D], circumferential shortening rate [Vcf] and end-diastolic diameter [Dd]) were obtained in 25 normal subjects and 37 patients with previously documented transmural myocardial infarction. The group with previous infarction demonstrated significant (P less than 0.001) differences from the normal group in each of the noninvasive measures. PEP/LVET and %deltaD were the most sensitive measures of left ventricular dysfunction. Deviation from the normal range in these measures occurred, respectively, in 70 and 65 percent of patients without dyspnea or fatigability (20 patients) and 85 percent of those without angina pectoris (13 patients). Abnormalities in systolic time interval and echocardiographic measures were related to the severity of dyspnea and fatigability but not to that of angina. Neither the presence of phonocardiographically documented third or fourth sound gallops nor an abnormal cardiothoracic ratio by chest roentgenogram reliably detected patients with abnormal left ventricular performance. The range of abnormality in left ventricular performance did not differ between patients with prior anterior or diaphragmatic myocardial infarction. The frequency of abnormal performance was greatest among patients with combined sites of prior infarction. Among 26 patients studied by coronary arteriography, abnormal left ventricular performance as determined by values for PEP/LVET and %deltaD occurred in fewer than 30 percent of those with 70 percent or greater obstruction of one coronary artery and in more than 80 percent of those with two or three vessel involvement. There was a high correlation between systolic time intervals, %delta D and Vcf, the closest correlation occurring between PEP/LVET and %deltaD (r = -0.93). These data document the sensitivity of the noninvasive systolic time intervals and echographic measures and their superiority over current clinical bedside methods in evaluating left ventricular performance in patients with prior myocardial infarction.

This study was undertaken to define the relation between the extent of left ventricular (LV) hypertrophy and ventricular systolic performance in patients with chronic systemic hypertension. Ninety patients with chronic systemic hypertension were compared with 41 normal subjects as determined by angiography. LV mass was estimated from the M-mode echocardiogram. Patients were separated into 3 groups: those with LV mass of less than 2 (group I, n = 58), 2 to 4 (group II, n = 21) and more than 4 (group III, n = 11) standard deviations above mean normal. The ratio of preejection period to LV ejection time (PEP/LVET), percent shortening of the echocardiographic internal diameter (% delta D) and velocity of circumferential shortening (Vcf) were used as indexes of LV systolic performance. The frequency of abnormality, expressed as percent of patients in groups I, II and III, was 33%, 55% and 85% for PEP/LVET, 15%, 35% and 72% for % delta D, and 0%, 15% and 55% for Vcf. For each group PEP/LVET was the most frequently abnormal measure and Vcf was the least frequent abnormality. Calculation of peak and end-systolic wall stress was used as an index of the adequacy of LV hypertrophy. This index was significantly reduced in group I, did not differ from control in group II and was significantly increased in group III, indicating that hypertrophy was appropriate to wall tension in groups I and II. It is concluded that the occurrence of LV dysfunction with increasing LV mass in patients with moderate LV hypertrophy (group I and II) reflects a deficiency in intrinsic contractile performance of the hypertrophied myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)

The positive inotropic effects and serum glycoside levels following intravenous and oral administration of betamethyl digoxin (BMD) were measured and compared with those of digoxin in normal adults. The cardiac inotropy was assessed noninvasively in the abbreviation of the electromechanical systolic index (QS2I) obtained by serial measurements of systolic time intervals. Following 0.8 mg BMD intravenously, the QS2I abbreviation occurred within 3 min and reached a maximum at 4 hr. The time-course and the magnitude of the response were essentially the same as those obtained with 0.8 mg digoxin given intravenously in the same subjects. The serum glycoside levels were also similar for both drugs. When administered orally the QS2I abbreviation to 0.8 mg BMD appeared at 40 min and reached a maximum at 4 hr. The time-course and the magnitude of the effects were similar to those observed following oral digoxin. The blood digitalis levels following the drug ingestion, however, were significantly higher for BMD than for digoxin which suggests greater gastrointestinal absorption of BMD. Based on our observations, the inotropic effects of BMD are similar to those of digoxin. Our results, however, do not demonstrate greater cardiac activity after oral administration of BMD despite higher blood levels.

The diagnosis of ruptured (perforated or torn) aortic valvular leaflets due to various causes has been made primarily at surgery or postmortem examination. Although angiocardiographic studies readily reveal aortic regurgitation, they rarely establish the presence of a ruptured aortic cusp as the cause of the aortic leak. Recent echocardiographic experience has brought to our attention seven patients with ruptured aortic valvular leaflets in whom the absenc of valvular vegetations was confirmed at surgery in six and at autopsy in one. The echocardiogram of the aortic root in these subjects revealed little or no increment in the diameter of the aortic root. In systole the usual box-like configuration of the leaflets, similar to that observed in normal subjects, was seen; however, in diastole the normal thin midaortic linear echoes were replaced by a thick band of echoes which often revealed high-frequency oscillations. In addition, high-frequency fibrations of the anterior mitral leaflet in diastole and increased systolic excursion of the interventricular septum and left ventricular posterior wall were observed.

In the normal population the duration of electrical systole (QT) is shorter (mean -26 +/- 13 ms, 1 standard deviation) than that of electromechanical systole (QS2), which it closely parallels throughout the range of resting heart rate. This close association prompted the hypothesis that the duration of QT may be more closely linked physiologically to QS2 than to the heart rate and hence may provide a more potent prognostic indicator than the relation of QT to heart rate. The present study was designed to test this hypothesis. On hundred stable patients 14 months after myocardial infarction were followed up an average of 43 months. Twenty patients had prolongation of QT relative to QS2 (QT greater than QS2) and 13 patients had long QT corrected for heart rate (QTc). There were 20 deaths (16 sudden). The cumulative 5 year survival rate was 35% in patients with QT greater than QS2 and 91% in patients with QT greater than or equal to QS2 (p less than 0.001). There was no significant difference in survival in patients with long QTc compared with patients with normal QTc (69 versus 82%). Univariate and multivariate analysis for the association of QT greater than QS2 with known risk factors, clinical descriptors, drug therapy, systolic time intervals (preejection period/left ventricular ejection time), and frequency of 1, 2 and 3 vessel coronary occlusive artery disease revealed that only the presence of abnormal preejection period/left ventricular ejection time added significantly to the presence of QT greater than QS2 in stratifying 5-year survival into high and low risk groups. Thus, in patients with coronary artery disease, the presence of QT greater than QS2 provides a new risk indicator that is more potent than QT corrected for heart rate.

Diastolic time (DT) is calculated as the cycle length (RR) minus electromechanical systole (QS2). The ratio of DT (RR-QS2) to RR interval times 100, or the percent diastole (%D), varies nonlinearly with heart rate (HR), increasing rapidly with decreasing HR. The effect of commonly used cardioactive agents on %D was studied in five groups of normal subjects. In group 1 (n = 12), propranolol (160 mg daily) increased %D from 55.9 +/- 1.7 to 64.7 +/- 1.3 (p less than 0.001) by slowing HR. In group 2 (n = 12), dobutamine (2.5 micrograms/kg/min) increased %D from 56.4 +/- 1.4 to 61.8 +/- 1.3 (p less than 0.005) by shortening the QS2. In group 3 (n = 10), Cedilanid-D (1.6 mg i.v.) increased %D from 55.5 +/- 1 to 63.2 +/- 0.7 (p less than 0.001), both by slowing the HR and shortening the QS2. In group 4 (n = 12), isoproterenol (2 micrograms/min) increased HR and shortened the QS2 significantly. The net result was a significant reduction of %D from 56.1 +/- 1.4 to 53.5 +/- 1.1, (p less than 0.05). In group 5 (n = 15), a 100-mg bolus of i.v. lidocaine did not have a significant effect on %D. This study indicates that cardiovascular drugs may have significant effects on the relative duration of diastole either by affecting HR or the duration of systole. This may have clinical implications for patients with coronary artery disease and patients with left ventricular hypertrophy, since in both cases coronary flow in mostly diastolic.

Determinations of systolic time intervals and echocardiographic measures of left ventricular performance were made in twenty-five normal subjects and 37 patients who had convalesced from a previous transmural myocardial infarction. On group analysis the patients with previous myocardial infarction demonstrated significant differences from the normals in each of the noninvasive measures. Among the noninvasive measures the PEP/LVET and deltaD% proved to be the most sensitive indicators of left ventricular dysfunction. Deviations from the normal range in PEP/LVET and deltaD% occurred in 65% to 70% of patients asymptomatic for dyspnea and fatigability (20 patients) and in 85% of patients asymptomatic for angina pectoris (13 patients). Neither the presence of phonocardiographically documented S3 or S4 or the finding of an abnormal C/T ratio on standard chest x-ray reliably detected patients with abnormal left ventricular performance. Among 26 patients studied by coronary arteriography, abnormal left ventricular performance by PEP/LVET and deltaD% occurred in less than 30% of those with obstruction (70% or greater) of one coronary artery and in over 80% of those with obstruction of two or three major arteries. A close correlation existed between the level of left ventricular performance measured by the PEP/LVET and the deltaD% (r = 0.93). These studies document the high degree of sensitivity of the noninvasive measures and demonstrate their superiority over clinical methods for detecting abnormal left ventricular performance in patients with previous myocardial infarction.

Among 22 patients with isolated mitral regurgitation of various origins, systolic time intervals (preejection period [PEP] index, left ventricular ejection time [LVET] index and PEP/LVET) and echocardiographic measures of left ventricular performance (end-diastolic diameter [Dd], end-systolic diameter [Ds], and the percent change in minor axis diameter [% delta D]) were calculated. The patients were classified into two groups, those with a normal or supernormal % delta D (group I, 15 patients) and those with a decreased % delta D (group II, 7 patients). On group analysis, prolongation of the preejection period, shortening of the left ventricular ejection time and an increase in PEP/LVET was generally characteristic of patients with mitral regurgitation. These changes were accentuated when mitral regurgitation was complicated by echocardiographic evidence of diminished left ventricular contractile performance (% delta D less than 30 percent). An increase in PEP/LVET to greater than 0.05 was consistently associated with abnormal left ventricular performance, whereas a normal PEP/LVET ratio reflected normal or supernormal left ventricular performance. An inverse linear relation was found between PEP/LVET and % delta D. When compared with previous data on the relation of these variables among patients without valve insufficiency, PEP/LVET proved to be increased for any level of % delta D in mitral regurgitation. The state of digitalization did not appear to influence the relation between PEP/LVET and % delta D. The use of echocardiographic measurements augments the determination of systolic time intervals in the analysis of left ventricular performance in patients with mitral regurgitation.

To test the safety and reliability of atrial pacing as a conversion technique in patients with atrial flutter who are receiving digitalis therapy, atrial pacing conversion was attempted for 49 episodes of atrial flutter in 32 consecutive patients. All patients except one were receiving digitalis. To control ventricular rates most patients had received larger than usual therapeutic doses of digitalis glycoside before pacing. Fourteen of the 25 patients whose serum levels were measured had glycoside concentrations greater than 2 ng/ml. Before atrial pacing the mean atrial and ventricular rates were, respectively, 290 +/- 20.6 and 134 +/- 27.9/min (mean +/- standard deviation). Successful rhythm conversion was achieved on 48 occasions (98%) in 31 patients. One patient required transthoracic direct current synchronized countershock cardioversion. With atrial pacing, the atrial flutter rhythm reverted immediately to sinus mechanism in 23 instances, and there were 25 episodes of atrial fibrillation. Among those who experienced atrial fibrillation, the rhythm spontaneously reverted to sinus mechanism within 24 hours on 14 occasions; on 11 occasions; the rhythm reverted to atrial flutter and repeat pacing was required. Sinus mechanism was eventually established in all 31 patients.

We studied the predictive accuracy and disparities among cineventriculographic ejection fraction, pre-ejection period over left ventricular ejection time (PEP/LVET) obtained from the systolic time intervals and the percent shortening of the internal echocardiographic diameter (% delta D) in assessing left ventricular performance in 453 consecutive patients without valvular heart disease. In 308 patients all three tests were normal, and in 78 patients all three tests were abnormal. Overall agreement (predictive accuracy) among ejection fraction (normal greater than or equal to 57), % delta D (normal greater than or equal to 28%) and PEP/LVET (normal less than or equal to 0.42) was 85%. In 67 patients disparities among the tests as measures of global left ventricular performance were found. The major mechanisms accounting for such disparities were: (a) large segmental contraction abnormalities which selectively distort the % delta D and ejection fraction and (b) diminished isovolumic pressure (less than 45 mmHg) which distorts PEP/LVET. When patients with segmental contraction abnormalities and low isovolumic pressure were excluded the agreement between PEP/LVET and ejection fraction was 97%, ejection fraction and % delta D 98% and PEP/LVET and % delta D 97%. The combined uses of systolic time intervals and echocardiogram minimizes error due to segmental contraction abnormalities and isovolumic pressure. If both PEP/LVET and % delta D are concordant the agreement with ejection fraction is 94% for normal and 99% for abnormal left ventricular function.

Twenty-five patients with chronic systemic hypertension were studied. Systolic time intervals and diastolic time were determined at baseline and after 12 weeks of therapy with nadolol, with or without bendroflumethiazide (treatment phase I), then after 12 weeks of therapy with hydralazine, bendroflumethiazide, or both (treatment phase II). Systolic, diastolic, and mean blood pressures were equally controlled after either treatment regimen. Heart rate was significantly slower after treatment phase I compared to baseline or after treatment phase II (p less than 0.001). Systolic time per minute was significantly shorter and diastolic time per beat and per minute were significantly longer after treatment phase I compared to baseline or after treatment phase II (p less than 0.001). Double and triple products decreased after either mode of therapy; however, these parameters were significantly lower after treatment phase I compared to treatment phase II (p less than 0.01). These changes in systolic and diastolic time and double and triple products may be of clinical significance during therapy of chronic systemic hypertension and may help explain the regression of left ventricular hypertrophy in patients with hypertension treated with sympathetic blocking agents.