Exercise-induced subendocardial dysfunction in dogs with left ventricular hypertrophy

The effects of treadmill exercise on regional myocardial blood flow and function were examined in 10 adult, conscious dogs with left ventricular hypertrophy (LVH) induced by aortic banding in puppies, which resulted in a left ventricular (LV) weight/body weight ratio of 8.5 +/- 0.3. Data were compared with results from eight control dogs with an LV weight/body weight ratio of 4.9 +/- 0.2. At rest, LV systolic and end-diastolic pressures were significantly greater (p less than 0.01), and mean arterial pressure was significantly less (p less than 0.05) in LVH dogs. Mean myocardial blood flow (control dogs, 0.98 +/- 0.11 ml/min/g; LVH dogs, 1.16 +/- 0.06 ml/min/g) and the transmural blood flow distribution at baseline, as assessed by endocardial/epicardial blood flow ratio (control, 1.35 +/- 0.12; LVH, 1.21 +/- 0.09), were similar in the two groups. During exercise to a target heart rate (240 beats/min), LVH dogs demonstrated greater (p less than 0.01) increases in LV systolic and end-diastolic pressures. In control dogs, as expected, exercise augmented velocity of circumferential fiber shortening (16 +/- 9%) and shortening fraction (15 +/- 5%), but in LVH dogs, exercise reduced the velocity of circumferential fiber shortening (-14 +/- 6%) and shortening fraction (-17 +/- 5%). Exercise also increased full wall thickening (35 +/- 5%), subendocardial wall thickening (66 +/- 10%), and subepicardial wall thickening (44 +/- 9%) in control dogs. In LVH dogs, exercise increased subepicardial wall thickening (31 +/- 9%) and reduced subendocardial wall thickening (-40 +/- 7%); full wall thickening did not change (-11 +/- 9%). This was associated with a fall in endocardial/epicardial flow ratio to 0.72 +/- 0.05 (p less than 0.01) in LVH dogs. The subendocardial dysfunction persisted late into recovery, at a time when the transmural blood flow distribution had returned to baseline; this occurrence suggested myocardial stunning. Thus, in dogs with LVH, selective subendocardial hypoperfusion and profound selective depression in subendocardial wall thickening are observed during exercise. The subendocardial dysfunction persisted into recovery despite resolution of the perfusion abnormality.     

Left ventricular systolic response to exercise in patients with systemic hypertension without left ventricular hypertrophy

Supine exercise radionuclide angiography was performed in 367 men to assess left ventricular (LV) systolic response to exercise; 58 had systemic hypertension without LV hypertrophy on a resting electrocardiogram and 309 were normotensive. All patients met the following criteria defining a low pretest likelihood of coronary artery disease: age less than 50 years; normal electrocardiographic response to exercise; absence of typical or atypical chest pain; and exercise heart rate greater than 120 beats/min. Patients taking beta-receptor blockers were excluded. There were no significant differences between hypertensive and normotensive groups in peak exercise heart rate, workload or exercise duration. However, hypertensive patients had significantly higher peak exercise systolic blood pressures and peak exercise rate-pressure products. There were no differences between patients with and without hypertension in resting ejection fraction, peak exercise ejection fraction (hypertensive patients 0.71 +/- 0.01, normotensive patients 0.70 +/- 0.05) or change in ejection fraction at peak exercise (hypertensive patients 0.07 +/- 0.01, normotensive patients 0.07 +/- 0.04). Diastolic and systolic ventricular volumes tended to be smaller in the hypertensive patients, but the difference was not statistically significant. The change in systolic volume with exercise was similar in the 2 groups (hypertensive -10 +/- 3 ml/m2, normotensive -10 +/- 1 ml/m2). In the absence of electrocardiographic evidence of LV hypertrophy, systemic hypertension does not influence LV systolic response to exercise.     

Exaggerated pressor response to treadmill exercise in chronic cocaine abusers with left ventricular hypertrophy.

BACKGROUND. Chronic cocaine abuse has been associated with a high prevalence of left ventricular hypertrophy (LVH) in normotensive individuals at rest. This study was conducted to determine whether chronic cocaine abusers with LVH would manifest an exaggerated pressor response to treadmill exercise. METHODS AND RESULTS. Forty-nine normotensive chronic cocaine abusers underwent Bruce protocol treadmill exercise testing until they attained 85% maximum predicted heart rate. A peak exercise systolic blood pressure greater than or equal to 210 mm Hg was defined as abnormal. In addition, they underwent two-dimensional echocardiography and had left ventricular mass determined by the area-length method. LVH was defined as left ventricular mass greater than or equal to 105 g/m2 and a posterior wall thickness greater than or equal to 1.2 cm. Age- and race-matched control subjects also underwent echocardiography and exercise testing. Group differences in peak exercise blood pressure in cocaine abusers with LVH, cocaine abusers without LVH, and control subjects were assessed by ANOVA. Groups were similar concerning age, race, heart rate, resting blood pressure, body surface area, and exercise duration. LVH was present in 16 of 49 (33%) cocaine abusers and three of 30 (10%) control subjects (p = 0.02). Of the 16 cocaine abusers with LVH, 10 (63%) had peak exercise blood pressures greater than or equal to 210 mm Hg, and three others had exercise blood pressures of 200 mm Hg. Therefore, peak exercise systolic blood pressure was significantly higher in cocaine abusers with LVH than in all other groups (p = 0.0001). CONCLUSIONS. Chronic cocaine abusers with LVH manifest an exaggerated pressor response to treadmill exercise. These data suggest that chronic cocaine abuse predisposes a subset of individuals to a heightened pressor response to a given sympathetic stimulus such as exercise and that this may contribute to the pathogenesis of LVH in chronic cocaine abusers.     

Patients with a hypertensive response to exercise have impaired systolic function without diastolic dysfunction or left ventricular hypertrophy

OBJECTIVES: We sought to determine if a hypertensive response to exercise (HRE) is associated with myocardial changes consistent with early hypertensive heart disease. BACKGROUND: An HRE predicts the development of chronic hypertension (HT) and may reflect a preclinical stage of HT. METHODS: Patients with a normal left ventricular (LV) ejection fraction and a negative stress test were recruited into three matched groups: 41 patients (age 56 +/- 10 years) with HRE (>210/105 mm Hg in men; >190/105 in women), comprising 22 patients with (HT+) and 19 without resting hypertension (HT-); and 17 matched control subjects without HRE. Long-axis function was determined by measurement of the strain rate (SR), peak systolic strain, and cyclic variation (CV) of integrated backscatter in three apical views. RESULTS: An HRE was not associated with significant differences in LV mass index. Exercise performance and diastolic function were reduced in HRE(HT+) patients, but similar in HRE(HT-) patients and controls. Systolic dysfunction (peak systolic strain, SR, and CV) was significantly reduced in HRE patients (p < 0.001 for all). These reductions were equally apparent in patients with and without a history of resting HT (p = NS) and were independent of LV mass index and blood pressure (p < 0.01). CONCLUSIONS: An HRE is associated with subtle systolic dysfunction, even in the absence of resting HT. These changes occur before the development of LV hypertrophy or detectable diastolic dysfunction and likely represent early hypertensive heart disease.     

Mechanisms for an abnormal radionuclide left ventricular ejection fraction response to exercise in patients with chronic, severe aortic regurgitation.

To clarify the mechanisms for an abnormal radionuclide left ventricular (LV) ejection fraction response to exercise in patients with chronic, severe aortic regurgitation (AR), we studied seven control patients and 21 patients with AR. We used exercise radionuclide angiography and catheterization of the right and left sides of the heart to obtain a calculation of LV chamber elastance. The control and AR groups had similar heart rates, systolic blood pressure responses to exercise, and exercise durations. In both patient groups, LV end-diastolic volume did not change with exercise. In contrast to the decrease in LV end-systolic volume (p less than 0.05) and increase in LV ejection fraction (p less than 0.01) in the control group, LV end-systolic volume in the patients with AR increased, resulting in little change in their LV ejection fraction. By stepwise multiple regression analysis, the radionuclide LV ejection fraction at peak exercise in patients with AR was determined by the LV chamber elastance, LV end-systolic volume, and stroke volume at peak exercise (cumulative r = 0.79, p less than 0.02); the change in radionuclide LV ejection fraction from rest to peak exercise was determined by the corresponding change in systemic vascular resistance, regurgitant index, and LV end-diastolic and end-systolic volumes (cumulative r = 0.88, p less than 0.02). These data demonstrate that in patients with AR, the radionuclide LV ejection fraction at peak exercise is principally determined by the cumulative effects of chronic, severe AR on LV systolic chamber performance, and the change in radionuclide LV ejection fraction from rest to peak exercise is principally established by peripheral vascular responses.     

Systolic and diastolic dysfunction during atrial pacing in conscious dogs with left ventricular hypertrophy

To determine the extent to which the hypertrophied left ventricle responds to the chronotropic stress induced by graded atrial pacing rates, we studied conscious, chronically instrumented dogs with severe compensated pressure overload left ventricular (LV) hypertrophy induced by aortic banding in puppies 8-10 weeks of age. At 1-2 years, dogs with severe LV hypertrophy (LV free wall/body wt ratio 6.8 +/- 0.6 g/kg) and sham-operated littermates (LV free wall/body wt ratio 4.0 +/- 0.3 g/kg) were instrumented with ultrasonic dimension crystals to measure LV short axis internal diameter and wall thickness, miniature LV pressure transducers, and aortic and LV catheters. During atrial pacing (240 beats/min) in eight control dogs, LV pressure did not change from 119 +/- 2 mm Hg, and mean velocity of circumferential fiber shortening (VCF) did not change from 1.25 +/- 0.09/sec. In seven dogs with LV hypertrophy, atrial pacing (240 beats/min) decreased systolic LV function; that is, LV systolic pressure decreased (p less than 0.01) by 65 +/- 12 from 254 +/- 14 mm Hg, and VCF decreased (p less than 0.01) by 0.19 +/- 0.03 from 0.97 +/- 0.15/sec. Diastolic dysfunction was also observed in the dogs with LV hypertrophy. In the control dogs during atrial pacing (240 beats/min), LV end-diastolic pressure decreased (p less than 0.01) by 8 +/- 1 from 9 +/- 1 mm Hg, end-diastolic stress decreased (p less than 0.01) by 18 +/- 2 from 22 +/- 2 g/cm2, and the radial myocardial stiffness constant did not change from 5.6 +/- 1.0.(ABSTRACT TRUNCATED AT 250 WORDS)     

Patterns of diastolic dysfunction in left ventricular hypertrophy.

The relative sensitivities of and interrelations between different measurements of diastolic function were studied in 50 patients with left ventricular hypertrophy diagnosed on anatomical grounds. Isovolumic relaxation time, the interval from minimum cavity dimension to mitral valve opening and relative dimension increase during this period, and the peak rate of dimension increase and wall thinning during rapid ventricular filling were measured by digitised M mode echocardiography. The relative heights of peak early diastolic and atrial velocities (a/E) and the time for decline of early diastolic velocity to half its peak value (velocity half time) were measured on continuous wave and pulsed Doppler and the relative height of the "a" wave was measured by apexcardiogram. All sets of values except those of the interval from minimum dimension to mitral opening were unimodally distributed, and all differed significantly from those in 20 age matched controls. The relative height of the "a" wave on the apexcardiogram (90% values were abnormal) was the most sensitive method of studying left ventricular diastolic function and peak rate of dimension increase was the least sensitive. Though none of the correlations was high, there were individual associations between peak rate of dimension increase, a/E, peak wall thinning rate, and velocity half time, and independently between delay in mitral valve opening and dimension change during this period. Other values seemed to be independent of one another, suggesting a different physiological basis. It is concluded that these various abnormal values do not reflect a single underlying disturbance of diastolic function. There are at least four possible discrete abnormalities: prolongation of isovolumic relaxation; incoordination during isovolumic relaxation; reduced rate of rapid filling; and an increase in the relative amplitude of the "a" wave probably caused by increased passive stiffness. These may be present singly or in combination in any patient.     

Effect of inotropic and vasodilator therapy on left ventricular diastolic filling in dogs with severe left ventricular dysfunction

Inotropic and vasodilator therapy for congestive heart failure improve left ventricular systolic performance by different mechanisms. However, the nature and extent to which diastolic filling is altered have not been well described. Acute severe left ventricular dysfunction was induced in 21 dogs by severe left ventricular global ischemia produced by left main coronary artery microsphere embolization until left ventricular end-diastolic pressure was greater than or equal to 18 mm Hg. Dobutamine was infused in seven dogs until the peak positive first derivative of left ventricular pressure (dP/dt) increased by greater than or equal to 33%. Nitroprusside was infused in seven dogs until left ventricular end-diastolic pressure was less than 15 mm Hg. Seven dogs were observed for 1 h after the induction of acute severe left ventricular dysfunction and served as the control group. In all groups of dogs, severe left ventricular dysfunction resulted in left ventricular dilation, reduction in area ejection fraction, elevation of left ventricular end-diastolic pressure and an early redistribution of diastolic filling (increased 1/3 and 1/2 filling fractions) despite a markedly abnormal time constant of relaxation. No changes were noted in any variable after 1 h of observation in the seven control dogs. Nitroprusside reduced left ventricular size and filling pressure, increased cardiac output, improved relaxation and redistributed diastolic filling to later in diastole as characterized by a reduced 1/3 filling fraction (19.4 +/- 7.4% versus 51.4 +/- 10%, p less than 0.001). The pressure-area curve was shifted downward and leftward.(ABSTRACT TRUNCATED AT 250 WORDS)     

Relation of obesity, high sodium intake, and eccentric left ventricular hypertrophy to left ventricular exercise dysfunction in essential hypertension

PURPOSE: To elucidate determinants of abnormal left ventricular functional responses to exercise in hypertensive patients. PATIENTS AND METHODS: One hundred twenty-seven patients with uncomplicated essential hypertension were studied by rest and exercise radionuclide angiography and by echocardiography at rest. RESULTS: The 24 patients with subnormal left ventricular ejection fraction at peak exercise (less than 54%) were similar in age and rest and exercise blood pressures to the 103 with normal exercise ejection fraction, but were more obese (p less than 0.005) and had greater left ventricular mass (p less than 0.03) and internal dimensions (p less than 0.001). The parallel increase in left ventricular chamber size and mass (eccentric hypertrophy) in the group of patients with exercise dysfunction was associated with higher resting end-systolic wall stress (p less than 0.001) and abnormal increases of end-systolic left ventricular volume from rest to peak exercise (p less than 0.001). Multivariate analysis revealed that exercise left ventricular dysfunction was independently associated with higher left ventricular mass (p less than 0.0005), end-systolic wall stress (p less than 0.001), dietary sodium intake (p less than 0.01), and body mass index (p less than 0.03). CONCLUSION: Among patients with uncomplicated essential hypertension, abnormal functional responses to exercise are strongly associated with eccentric ventricular hypertrophy, obesity, and high sodium intake.     

Relationship between blood pressure response during exercise and tendency to left ventricular hypertrophy

From among subjects who were examined by submaximal exercise testing in 1987, 54 were selected in order to examine the relationship between the blood pressure response during exercise and the tendency to develop left ventricular hypertrophy. Only those subjects having resting systolic blood pressure values between 120 mmHg and 140 mmHg were selected. The maximum systolic blood pressure during submaximal exercise was highly correlated with the sum of the R wave amplitude in V5 and the S wave amplitude in V1 of the resting ECG (r = 0.496, p less than 0.001, n = 54), as well as with the left ventricular mass normalized for body surface area (r = 0.609, p less than 0.005, n = 23). The maximum systolic blood pressure measured during submaximal exercise did not correlate with age or exercise duration. These results suggest that a greater blood pressure response during exercise is related to the tendency to develop left ventricular hypertrophy.     

Value of left atrial function in predicting exercise capacity in heart failure with moderate to severe left ventricular systolic dysfunction

Left atrial (LA) function is associated with left ventricular (LV) diastolic filling and cardiac output response to exercise. But the relation between LA function and exercise performance has not been adequately evaluated. The aim of this study was to investigate the relation between LA function and exercise capacity in dilated cardiomyopathy (DCM) with cardiopulmonary exercise testing. Forty-four patients with a left ventricular end-diastolic dimension (LVDd) > or = 60 mm and an ejection fraction (EF) < or = 40%, and in normal sinus rhythm were included in this study. Patients were divided into group 1 and group 2 according to their exercise peak oxygen uptake (VO2) (group 1: peak VO2 >14 mL/kg/min, group 2: peak VO2 < or = 14 mL/ kg/min). LA function indices were defined as follows: LA end-systolic diameter (LASd), end-diastolic diameter (LADd), LA systolic volume (LASV), LA diastolic volume (LADV), LA ejection volume (LAEV), and LA ejection fraction (LAEF). LASd, LADd, LASV, and LADV were significantly increased in group 2 (P < 0.001, P < 0.001, P < 0.05, P < 0.005). Group 1 had significantly higher LAEF (P < 0.001 ) and LVEF (P < 0.05). Group 2 had significantly shorter exercise duration, and decreased anaerobic threshold levels and minute ventilation volumes (P < 0.001, P < 0.001, P < 0.005 ). There was a positive correlation between peak VO2 and LVEF (r = 0.46, P = 0.002), and LAEF (r = 0.61, P < 0.001), peak A wave velocity (r = 0.39, P = 0.009), E wave deceleration time (r = 0.56, P < 0.001), and isovolumic relaxation time (IVRT) (r = 0.35, P = 0.04). There was a negative correlation between peak VO2 and LASd (r = -0.53, P < 0.001) LADd (r = -0.59, P < 0.001), LASVI (r = -0.34, P = 0.027), LADVI (r = -0.37, P = 0.001), and the E/A ratio (r = -0.41, P = 0.006), Decreased LAEF and increased LA sizes were associated with decreased peak VO2. The results clearly demonstrate that LA functions at rest are related to exercise performance in patients with heart failure.     

Patterns of diastolic dysfunction in left ventricular hypertrophy

The relative sensitivities of and interrelations between different measurements of diastolic function were studied in 50 patients with left ventricular hypertrophy diagnosed on anatomical grounds. Isovolumic relaxation time, the interval from minimum cavity dimension to mitral valve opening and relative dimension increase during this period, and the peak rate of dimension increase and wall thinning during rapid ventricular filling were measured by digitised M mode echocardiography. The relative heights of peak early diastolic and atrial velocities (a/E) and the time for decline of early diastolic velocity to half its peak value (velocity half time) were measured on continuous wave and pulsed Doppler and the relative height of the "a" wave was measured by apexcardiogram. All sets of values except those of the interval from minimum dimension to mitral opening were unimodally distributed, and all differed significantly from those in 20 age matched controls. The relative height of the "a" wave on the apexcardiogram (90% values were abnormal) was the most sensitive method of studying left ventricular diastolic function and peak rate of dimension increase was the least sensitive. Though none of the correlations was high, there were individual associations between peak rate of dimension increase, a/E, peak wall thinning rate, and velocity half time, and independently between delay in mitral valve opening and dimension change during this period. Other values seemed to be independent of one another, suggesting a different physiological basis. It is concluded that these various abnormal values do not reflect a single underlying disturbance of diastolic function. There are at least four possible discrete abnormalities: prolongation of isovolumic relaxation; incoordination during isovolumic relaxation; reduced rate of rapid filling; and an increase in the relative amplitude of the "a" wave probably caused by increased passive stiffness. These may be present singly or in combination in any patient.     

Regional left ventricular diastolic dysfunction in patients with apical hypertrophy

Differences in cardiac function between the apical and the chordal parts of the left ventricle in apical hypertrophy (APH) were investigated by M-mode echocardiography. The subjects consisted of 10 patients with APH (APH Group) and 10 normal controls (N Group). The M-mode echocardiograms of the interventricular septum (IVS) and left ventricular posterior wall (LVPW), both in the apical and chordal parts were simultaneously recorded with the electrocardiogram and phonocardiogram. There were no significant differences in the blood pressures, heart rates, left ventricular end-diastolic internal diameters, and left ventricular end-systolic internal diameters between the APH Group and the N Group. The hypertrophy was localized to the IVS and LVPW of the apical part in the APH Group. In the chordal part, there were no significant differences in the peak negative dD/dt (-dD/dt) and the time to the peak filling rate (TPFR) between the APH Group and N Group. In the apical part, -dD/dt of the APH Group tended to increase compared with that of the N Group. The TPFR of the APH Group was significantly longer than that of the N Group (APH Group: 167 +- 33 msec and N Group: 126 +- 19 msec, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)     

Impact of left ventricular hypertrophy on blood pressure responses to exercise.

It is claimed that exaggerated blood pressure (BP) responses to exercise are predictive of future hypertension and may also be indicative of left ventricular (LV) hypertrophy. The relation between LV hypertrophy and maximal exercise BP was examined in 35 normal male volunteers and 65 untreated hypertensive male patients. Multiple stepwise regression analysis revealed that preexercise systolic BP was the major determinant of maximal exercise systolic BP (r = 0.52; p less than or equal to 0.0001), indicating that higher baseline BP predicted higher exercise BP. However, hypertensive patients with LV hypertrophy had the smallest increases in systolic BP with exercise. Accordingly, there was an inverse relation between LV muscle mass and systolic BP responses to exercise in these patients (r = -0.34; p = 0.005). When compared with normotensive subjects, hypertensive patients had lower measures of maximal oxygen uptake and exercise heart rates (p = 0.01). This may indicate lower cardiac performance at maximal exercise and explain the reduced capacity of hypertensive patients with LV hypertrophy to increase systolic BP with exercise. Neither baseline nor exercise BPs correlated with LV mass; instead, the model of regression analysis indicated that body weight was the principal determinant of LV mass. Contrary to previous reports, exaggerated exercise BPs were not associated with LV hypertrophy in hypertensive or normotensive patients.     

Progressive left ventricular remodeling in patients with hypertrophic cardiomyopathy and severe left ventricular hypertrophy

OBJECTIVES: The aim of this study was to determine the natural history of patients with hypertrophic cardiomyopathy (HCM) and severe left ventricular hypertrophy (LVH) (i.e., maximal left ventricular wall thickness [MLVWT] >/=30 mm) and whether changes in cardiac morphology influence the course of the disease. BACKGROUND: Severe LVH is common in young and rare among elderly patients with HCM. This has been explained by a high incidence of sudden death. We hypothesized that this age-related difference might be explained by left ventricular wall thinning. METHODS: A total of 106 (age 33 +/- 15 years; 71 males) consecutive patients with severe LVH underwent history taking, examination, electrocardiography, echocardiography, cardiopulmonary exercise testing, and Holter analysis. Survival data were collected at subsequent clinic visits or by communication with patients and their general practioners. In order to assess morphologic and functional changes, 71 (67.0%) patients (mean age 31 +/- 15 years; 47 males) followed at our institution underwent serial (>/=1 year) assessment. RESULTS: Of the 106 patients, the majority (78 [71.6%]) were <40 years of age. During follow-up (92 +/- 50 months [range 1 to 169]), 18 (17.0%) patients died or underwent heart transplantation (13 sudden cardiac deaths, 2 heart failure deaths, 1 heart transplantation, 1 stroke, 1 postoperative death). Five-year survival from sudden death was 90.1% (95% confidence interval [CI] 84.0% to 96.3%), and that from heart failure death or transplantation was 97.7% (95% CI 94.5 to 100). In patients serially evaluated over 85 +/- 51 months, there was an overall reduction in MLVWT of 0.6 mm/year (95% CI 0.31 to 0.81, p = 0.00004). Wall thinning >/=5 mm was observed in 41 patients (57.7%; age 35 +/- 13 years; 28 males). On multivariate analysis, the follow-up duration only predicted wall thinning (0.6 mm/year, 95% CI 0.38 to 0.85, p < 0.00001). CONCLUSIONS: Left ventricular remodeling is common in patients with severe LVH and contributes to the low prevalence of severe LVH seen in middle age and beyond.     

Progression from concentric left ventricular hypertrophy and normal ejection fraction to left ventricular dysfunction

Concentric left ventricular (LV) hypertrophy develops in response to a chronically increased LV afterload and is associated with increased cardiovascular events. Although the progression to systolic and diastolic heart failure is a known consequence of LV hypertrophy, few data are available on the frequency of deterioration to systolic dysfunction in patients with LV hypertrophy who originally had a normal LV ejection fraction. We evaluated the baseline and follow-up characteristics in 1,024 patients with concentric LV hypertrophy and a normal ejection fraction who had paired echocardiograms that were separated by ≥1 year. Systolic dysfunction occurred in 134 patients (13%) after a mean follow-up of 33 ± 24 months. The most common associated variable was interval myocardial infarction, which occurred in 43% of patients. Other risk factors for developing LV systolic dysfunction included QRS prolongation (>120 ms) and elevated follow-up arterial impedance defined as a value >4.0 mm Hg/ml/m(2). Patients with either a prolonged QRS interval or an elevated follow-up arterial impedance had twice the likelihood of developing LV systolic dysfunction, and, if both factors were present, there was a greater than fourfold increased risk of developing systolic dysfunction. Blood pressure measurements alone did not adequately reflect an elevated arterial impedance. In conclusion, 13% of patients with a normal ejection fraction and concentric LV hypertrophy progress to systolic dysfunction during approximately 3 years of follow-up. The risk factors for loss of function were interval myocardial infarction, prolonged QRS, and chronically elevated arterial impedance.     

Hemodynamic and metabolic basis of impaired exercise tolerance in patients with severe left ventricular dysfunction

Hemodynamic and metabolic changes were measured at rest and during exercise in 23 patients with chronic heart failure and in 6 control subjects. Exercise was limited by leg fatigue in both groups and capacity was 40% lower in the patients with failure. At rest, comparing patients with control subjects, heart rate and right atrial and pulmonary wedge pressure were higher; cardiac output, stroke volume and work indexes and ejection fraction were lower; mean arterial and right atrial pressure and systemic resistance were similar. During all phases of exercise in patients with heart failure, pulmonary wedge pressure and systemic vascular resistance were higher and pulmonary vascular resistance remained markedly elevated compared with values in control subjects. Cardiac output was lower in the patients with failure, but appeared to have the same physiologic distribution in both groups during exercise. Although arterial-femoral venous oxygen content difference was higher in patients with heart failure, this increase did not compensate for the reduced blood flow. Even though the maximal oxygen consumption was significantly reduced, femoral venous lactate and pH values were higher than values in control subjects, but femoral venous pH was similar in both groups at their respective levels of maximal exercise. Ejection fraction was lower in those with heart failure at rest and did not increase with exercise. Ventilation in relation to oxygen consumption was higher in patients with failure than in control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prognostic importance of the immediate hemodynamic response to nifedipine in patients with severe left ventricular dysfunction

To determine the clinical significance of the occurrence of hemodynamic deterioration after the administration of calcium channel blocking drugs, nifedipine (20 mg orally) was administered to 29 patients with severe left ventricular dysfunction. Thirteen patients showed hemodynamic improvement with the drug (Group 1), as shown by a notable increase in cardiac index associated with a modest decrease in mean arterial pressure. The other 16 patients exhibited hemodynamic deterioration after nifedipine (Group 2), as reflected by a decline in right and left ventricular stroke work indexes accompanied by a marked hypotensive response. These differences were not related to differences in the peripheral vascular response to nifedipine, because both groups showed similar decreases in systemic and pulmonary vascular resistances. Groups 1 (hemodynamic improvement) and 2 (hemodynamic deterioration) were similar with respect to all demographic variables and pretreatment left ventricular performance (cardiac index, left ventricular filling pressure and systemic vascular resistance). Yet, the 1 year actuarial survival in patients in Group 1 was substantially better than that in patients in Group 2 (67 versus 23%, p = 0.009). Group 2, however, had higher values for plasma renin activity (17.7 +/- 6.0 versus 4.3 +/- 1.4 mg/ml per h, p less than 0.05), lower values for serum sodium concentration (134.6 +/- 1.2 versus 139.2 +/- 0.6 mEq/liter, p less than 0.05) and higher values for mean right atrial pressure (15.8 +/- 2.0 versus 7.9 +/- 1.4 mm Hg, p less than 0.01) than did patients in Group 1.(ABSTRACT TRUNCATED AT 250 WORDS)