Regression of myocardial hypertrophy: electrocardiographic-echocardiographic correlations after aortic valve replacement in patients with chronic aortic regurgitation

Serial electrocardiographic and echocardiographic left ventricular (LV) studies were performed in 21 patients before and after aortic valve replacement (AVR) for chronic aortic regurgitation. Changes in voltage (SV1 + RV5-6) after AVR were assessed and evaluated relative to changes in LV mass. Muscle cross-sectional area (CSA) derived from echocardiographic dimension and wall thickness data was used as an index of LV muscle mass (LV hypertrophy greater than 10 cm2/m2). In 15 patients, voltage was reduced after AVR: Seven had normal voltage (48 +/- 17 mm to 25 +/- 6 mm, p less than 0.005) and eight still had increased voltage (61 +/- 17 mm to 40 +/- 4 mm, p less than 0.01). Patients with normal voltage had complete regression of hypertrophy by echocardiography (CSA decreased from 13 +/- 3 cm2/m2 to 9 +/- 1 cm2/m2, p less than 0.025), while those who had persistently increased voltage had incomplete regression (15 +/- 2 cm2/m2, p less than 0.001). Reduction in voltage generally occurred in the first 6 months after AVR. Three patients with unchanged voltage had evidence of paraprosthetic regurgitation and minimal change in CSA. Three other patients with voltage had evidence of paraprosthetic regurgitation and minimal change in CSA. Three other patients with persistent LV enlargement without paraprosthetic regurgitation had a severe intraventricular conduction delay. Data from 59 electrocardiographic-echocardiographic studies before and after AVR revealed a strong correlation (r = 0.81) between voltage and muscle CSA. After surgical correction of chronic aortic regurgitation, regression of LV hypertrophy can be assessed by serial electrocardiographic studies. These ECG data identify patients with complete, incomplete or no regression of LV hypertrophy.     

Regression of coronary artery dimensions after successful aortic valve replacement.

BACKGROUND. The effect of regression of myocardial hypertrophy on coronary artery dimensions was evaluated in patients with aortic valve disease who underwent valve replacement. METHODS AND RESULTS. Cross-sectional area (CSA) of the three major coronary arteries (left anterior descending [LAD], left circumflex [LCx], and right coronary artery) was determined by quantitative coronary arteriography in 15 patients with aortic valve disease before and 38 months (range, 14-113 months) after successful aortic valve replacement. Twelve normal subjects served as controls. Left ventricular (LV) angiographic mass was calculated according to the method of Rackley. CSA of the left coronary artery was larger in aortic valve disease than in controls (LAD, 15 versus 8 mm2, p less than 0.001; LCx, 14 versus 6 mm2, p less than 0.001). After valve replacement, CSA of the left coronary artery decreased (LAD, 12 mm2, p less than 0.05 versus before surgery; LCx, 11 mm2, p less than 0.05 versus before surgery) but remained significantly larger than in controls. CSA of the right coronary artery in patients with aortic valve disease was not different from controls. LV muscle mass was significantly increased in aortic valve disease patients before (364 g) and after (250 g) valve replacement compared with controls (135 g). The appropriateness of coronary artery size with respect to muscle mass was evaluated by normalizing CSA of the left coronary artery (LAD + LCx) per 100 g of LV muscle mass (mm2/100 g). This index amounted to 11 mm2/100 g in controls, to 8 mm2/100 g in preoperative patients (p less than 0.05 versus controls), and to 10 mm2/100 g in postoperative patients with aortic valve disease (p = NS versus controls). CONCLUSIONS. In patients with aortic valve disease, CSA of the proximal LAD and LCx is increased, but this increase is not sufficient to keep CSA per 100 g of LV mass within normal limits. The postoperative decrease in muscle mass is associated with a decrease in the size of LAD and LCx, whereas the size of the right coronary artery remains unchanged. In contrast to the preoperative state, the residually hypertrophied LV myocardium after aortic valve replacement is supplied by an enlarged but adequately sized LAD and LCx.     

Coronary vascular reserve in left ventricular hypertrophy secondary to chronic aortic regurgitation

Coronary vascular reserve was studied in 11 patients with severe chronic aortic regurgitation (AR). Nineteen patients with the chest pain syndrome and normal findings on cardiac catheterization served as control subjects. Resting coronary sinus flow and contrast-agent-induced hyperemia were measured by continuous thermodilution. Left ventricular (LV) dimensions and mass were obtained echocardiographically. All patients had normal coronary arteries. Resting coronary flow was increased and coronary reserve was decreased in patients with AR compared with the control subjects: 310 +/- 38 versus 121 +/- 13 ml/min and 56 +/- 9 versus 86 +/- 7.5%, respectively. The decrease in coronary vascular reserve correlated with the increase in LV mass (r = -0.86, p = 0.001) and LV wall thickness (r = -0.83, p = 0.002) and with the decrease in LV volume/mass ratio (r = 0.761, p = 0.007). There was no significant correlation between the decrease in coronary vascular reserve and LV volume (r = 0.255), LV peak wall stress (r = 0.292), LV systolic pressure (r = -0.495), aortic or LV diastolic pressure (r = 0.322 and -0.318, respectively), or aortic-LV diastolic gradient, nor with the voltage on the electrocardiogram (limb leads r = -0.60, precordial leads r = -0.118). Thus, coronary vascular reserve is decreased in proportion to the degree of left ventricular hypertrophy in patients with chronic AR. Patients with angina pectoris tended to have a lower coronary vascular reserve than those without angina (median 26 versus 76%, difference not significant). LV wall thickness and not LV volume is the critical component of left ventricular mass related to coronary reserve. No significant correlation between the decrease in coronary vascular reserve and the presence of angina pectoris was demonstrated.     

Coronary flow studies in patients with left ventricular hypertrophy of the hypertensive type. Evidence for an impaired coronary vascular reserve

Increased myocardial blood flow occurs in ventricular hypertrophy, but flow per 100 grams of myocardium remains normal. The increase in flow may be obtained at the expense of the existing coronary vascular reserve or by an increase in the vascular bed. The coronary vascular reserve was studied by analyzing the hyperemic reaction to selective injection of contrast agent into the coronary arteries in 25 patients: a control group (9 patients) with chest pain syndrome, normal coronary arteries and a normal left ventricle (Group I) and 16 patients with aortic stenosis, left ventricular hypertrophy and normal coronary arteries (Group II). The hyperemic response in Groups I and II was 73.3 +/- 2.2 and 65.8 +/- 9.1 percent, respectively (difference not significant). Group II was subdivided into two groups: Group IIA had five patients with a left ventricular mass of less than 200 g (mean 158.8 +/- 25.9); this group had a hyperemic response of 102.3 +/- 9.9 percent. Group IIB had 11 patients with a left ventricular mass of more than 200 g (mean 308.9 +/- 22.5) and a hyperemic response of 49.27 +/- 10.42 percent. The hyperemic response was correlated with the diastolic left ventricular-aortic gradient (r = +0.64, p less than 0.001), left ventricular mass (r = -0.51, p less than 0.01) and aortic diastolic pressure (r = +0.636, p less than 0.001). Group I had a left ventricular mass similar to that of Group IIA (124.9 +/- 9 and 158.8 +/- 26 g, respectively) but a lower hyperemic response (73.3 +/- 2 and 102.3 +/- 10 percent, respectively). These data suggest that severe left ventricular hypertrophy is associated with a reduction in coronary vascular reserve; it is speculated that this decrease in the vascular reserve capacity may be related to the ischemic component of hypertrophic heart disease.     

Comparison of proximal left anterior descending and circumflex coronary artery dimensions in aortic valve stenosis and hypertrophic cardiomyopathy

To examine the "adequacy" of basal coronary flow in ventricular hypertrophy, the relation between proximal coronary artery dimensions and regional ventricular mass in aortic valve stenosis (AS) and hypertrophic cardiomyopathy (HC) was evaluated. Coronary artery size was determined by quantitative coronary arteriography while global/regional ventricular mass was calculated using computer-processed biplane 2-dimensional echocardiography. In comparison to 18 "normal" subjects, left anterior descending coronary dimensions were significantly larger in those with hypertrophy (normal 3.32 +/- 0.54, AS 3.82 +/- 0.71, HC 4.72 +/- 0.81 mm, p less than 0.05), with progressive increases in left anterior descending/circumflex coronary diameter ratios (normal 1.04 +/- 0.14, AS 1.18 +/- 0.19, HC 1.25 +/- 0.31, p less than 0.01). Compared to the AS group, indexed anteroseptal mass was greater in the HC subjects (AS 40.9 +/- 8.9 vs HC 72.1 +/- 21 g/m2, p less than 0.001). Both septal width/left anterior descending coronary diameter ratios (AS 3.61 +/- 1.06 vs HC 4.85 +/- 1.17 mm/mm, p less than 0.05) and indexed anteroseptal mass/left anterior descending coronary diameter ratios (AS 11.2 +/- 3.0 vs HC 15.6 +/- 3.4 g/m2/mm, p less than 0.01) were greater in HC subjects. Increased coronary dimensions were observed in both AS and HC, with the greatest changes noted within the left anterior descending distribution in HC, but when analyzed with respect to regional ventricular mass, these subjects demonstrated relative "inadequate" enlargement in coronary artery diameters. Underdeveloped epicardial coronary arteries may contribute to anteroseptal myocardial ischemia, with resultant angina pectoris, increased ventricular ectopic activity and sudden death in HC.     

Assessment of atrioventricular conduction in aortic valve disease.

To determine the frequency of atrioventricular conduction disturbances in aortic valve disease, 26 consecutive patients (age 54 +/- 2 years) with symptomatic aortic valve disease were studied by His bundle electrocardiography at the time of cardiac catheterisation and were compared with a group of patients who underwent cardiac catheterisation and were found to have coronary artery or mitral valve disease but no aortic valve disease. Patients with aortic valve disease had significantly longer PR, AH, and HV intervals than cardiac patients not having this abnormality. Patients with aortic stenosis had prolonged HV, 52 +/- 6 vs +/- 42 +/- 2 ms (P = 0.06), whereas patients with chronic aortic regurgitation had prolonged PR, 245 +/- 27 vs 163 +/- 5 ms (P less than 0.001), and prolonged AH, 178 +/- 30 vs 102 +/- ms (P less than 0.001). Patients with combined lesions had significant prolongation of PR, AH, and HV intervals. Three patients with acute aortic regurgitation caused by endocarditis had normal atrioventricular conduction. Though the presence of valvular calcification did not significantly alter the pattern of atrioventricular conduction in these patients, those with calcified aortic valves had longer HV (P less than 0.005) than the control group. In addition, ventricular dysfunction or coronary artery disease did not affect the pattern of atrioventricular conduction in these patients. Thus, atrioventricular conduction disturbances are common in symptomatic aortic valve disease. With aortic stenosis the site of delay occurs more frequently below the His deflection, whereas in aortic regurgitation it is more frequent above the His deflection.     

Assessment of atrioventricular conduction in aortic valve disease

To determine the frequency of atrioventricular conduction disturbances in aortic valve disease, 26 consecutive patients (age 54 +/- 2 years) with symptomatic aortic valve disease were studied by His bundle electrocardiography at the time of cardiac catheterisation and were compared with a group of patients who underwent cardiac catheterisation and were found to have coronary artery or mitral valve disease but no aortic valve disease. Patients with aortic valve disease had significantly longer PR, AH, and HV intervals than cardiac patients not having this abnormality. Patients with aortic stenosis had prolonged HV, 52 +/- 6 vs +/- 42 +/- 2 ms (P = 0.06), whereas patients with chronic aortic regurgitation had prolonged PR, 245 +/- 27 vs 163 +/- 5 ms (P less than 0.001), and prolonged AH, 178 +/- 30 vs 102 +/- ms (P less than 0.001). Patients with combined lesions had significant prolongation of PR, AH, and HV intervals. Three patients with acute aortic regurgitation caused by endocarditis had normal atrioventricular conduction. Though the presence of valvular calcification did not significantly alter the pattern of atrioventricular conduction in these patients, those with calcified aortic valves had longer HV (P less than 0.005) than the control group. In addition, ventricular dysfunction or coronary artery disease did not affect the pattern of atrioventricular conduction in these patients. Thus, atrioventricular conduction disturbances are common in symptomatic aortic valve disease. With aortic stenosis the site of delay occurs more frequently below the His deflection, whereas in aortic regurgitation it is more frequent above the His deflection.     

Effect of mitral regurgitation on diastolic filling with left ventricular hypertrophy

Earlier studies have suggested that mitral regurgitation (MR) augments early left ventricular (LV) diastolic filling. To determine whether MR affects early diastolic filling in patients with abnormal diastolic filling, transmitral pulsed-wave Doppler recordings were used to study 32 normal subjects, 21 patients with LV hypertrophy, 23 with LV hypertrophy and MR and 15 patients with MR. Patients with MR had increased peak early filling velocities (MR 108 +/- 27 cm/s, normal 80 +/- 16 cm/s, p less than 0.01), peak atrial filling velocities (MR 72 +/- 18 cm/s, normal 55 +/- 12 cm/s, p less than 0.05) and increased deceleration rates (MR 5.0 +/- 1.9 m/s2, normal 3.5 +/- 1.2 m/s2, p less than 0.05). Patients with LV hypertrophy had reduced peak early filling velocities (69 +/- 14 cm/s, p less than 0.05) and increased peak atrial filling velocities (83 +/- 16 cm/s, p less than 0.001). There was also an increase in the atrial filling fraction and reduction in the rapid filling fraction as compared with normal patients. Patients with LV hypertrophy and MR had increased peak early filling velocities (98 +/- 26 cm/s, p less than 0.01 vs normal, p less than 0.001 vs LV hypertrophy patients), increased atrial filling velocities (84 +/- 27 cm/s, p less than 0.001 vs normal), increased deceleration rates (4.4 +/- 2.4 m/s2, p less than 0.05 vs normal) and a normal distribution of diastolic filling. Within the LV hypertrophy and MR group, diastolic filling parameters were similar when patients were subgrouped on the basis of auscultability of MR. MR augments early diastolic filling and may tend to normalize diastolic filling patterns in LV hypertrophy patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

Geometric and functional correlates of electrocardiographic repolarization and voltage abnormalities in aortic regurgitation

Although electrocardiographic left ventricular hypertrophy is a recognized marker of disease severity in patients with chronic aortic regurgitation, the quantitative relations of repolarization abnormalities and QRS voltage to measurements of cardiac structure and function have not been established. The presence or absence of the "strain" pattern of repolarization and QRS voltage was compared with echocardiographic and radionuclide cineangiographic findings in 95 adults with sever, pure, chronic aortic regurgitation and no evidence of coronary artery disease. In contrast to 54 patients with normal repolarization, 41 patients with an abnormal repolarization pattern had greater left ventricular end-diastolic and end-systolic dimensions (7.2 +/- 1.1 versus 6.6 +/- 0.8 cm, p less than 0.002 and 5.2 +/- 1.2 versus 4.4 +/- 0.7, p less than 0.001, respectively), greater left ventricular mass (431 +/- 138 versus 303 +/- 89 g, p less than 0.001), higher end-systolic stress (128 +/- 46 versus 95 +/- 27 dynes-cm2 X 10(3), p less than 0.001), lower fractional shortening (28 +/- 8 versus 34 +/- 5%, p less than 0.001) and lower exercise ejection fraction (39 +/- 11 versus 51 +/- 8%, p less than 0.001). Multiple logistic regression analysis revealed that left ventricular mass and end-systolic stress were independently related to the presence of repolarization abnormalities (p less than 0.005). Among the 73 asymptomatic patients, those with normal repolarization had significantly lower prevalences of fractional shortening less than 25% (1 of 45 versus 5 of 27, p less than 0.05), left ventricular systolic dimension greater than 5.5 cm (1 of 45 versus 8 of 27, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Coronary flow and resistance reserve in patients with chronic aortic regurgitation, angina pectoris and normal coronary arteries

Left ventricular hypertrophy has been found to be associated with a reduction of coronary vascular reserve, which could be responsible for episodes of myocardial ischemia. To evaluate coronary flow and resistance reserve in patients with chronic aortic regurgitation, coronary sinus blood flow and coronary resistance were measured before and after an intravenous dipyridamole infusion (0.14 mg/kg per min X 4 min) in eight control subjects and eight patients with aortic regurgitation, exertional angina pectoris and normal coronary arteriograms. Coronary flow reserve, evaluated by the dipyridamole/basal coronary sinus blood flow ratio, and coronary resistance reserve, evaluated by the basal/dipyridamole coronary resistance ratio, were both significantly reduced in patients with aortic regurgitation (1.67 +/- 0.40 versus 4.03 +/- 0.52 in control subjects, p less than 0.001 and 1.71 +/- 0.50 versus 4.38 +/- 0.88 in control subjects, p less than 0.001, respectively). In patients with aortic regurgitation, basal coronary sinus blood flow was higher than in control subjects (276 +/- 81 versus 105 +/- 24 ml/min, respectively, p less than 0.001) and basal coronary resistance was lower (0.31 +/- 0.13 versus 0.95 +/- 0.17 mm Hg/ml per min, respectively, p less than 0.001), but coronary blood flow and resistance after dipyridamole were not significantly different in the two groups (461 +/- 159 versus 418 +/- 98 ml/min in control subjects, 0.19 +/- 0.11 versus 0.22 +/- 0.04 mm Hg/ml per min in control subjects, respectively). These data demonstrate that coronary reserve is severely reduced in patients with chronic aortic regurgitation and exertional angina.(ABSTRACT TRUNCATED AT 250 WORDS)     

Reduction of systolic coronary blood flow in experimental left ventricular outflow tract obstruction

In aortic valvular stenosis, coronary reserve has been shown to be markedly diminished despite normal coronary arteries. To gain further insight into this phenomenon, we examined the effects of an acute subaortic valvular obstruction on coronary blood flow (CBF) in seven open-chest anesthetized dogs. Transient subaortic obstruction was produced by inflating a catheter-tip balloon in the left ventricular (LV) outflow tract. The degree of obstruction, a 26 +/- 3 mm Hg gradient across the aortic valve, was adjusted to achieve an elevation of LV pressure while maintaining a constant aortic pressure (coronary perfusion pressure). In seven dogs with intact coronary vasomotor tone, systolic left anterior descending CBF decreased from 20 +/- 9 ml/min during the control period to 13 +/- 3 ml/min during subaortic obstruction (p less than 0.001). Diastolic CBF increased from 52 +/- 9 to 58 +/- 10 ml/min (p less than 0.05), and total CBF remained unchanged. In three dogs with maximal coronary vasodilation, systolic CBF decreased during subaortic obstruction, diastolic CBF remained unchanged, and total CBF decreased. The present data suggest that elevation of LV intracavitary pressure above coronary perfusion pressure can reduce systolic CBF and lead to an autoregulatory compensation that taxes coronary flow reserve.     

Relationship of atrial natriuretic factor to left ventricular volume and mass

Although atrial natriuretic factor is primarily of atrial origin, recent observations indicate that the hormone is also synthesized by hypertrophied left ventricular myocardium. To assess the separate influences of left ventricular and left atrial dilatation and left ventricular hypertrophy on human atrial natriuretic factor levels, left atrial dimension and volume and left ventricular dimension and mass were compared in 49 normal subjects, in 33 patients with chronic aortic regurgitation, and in 15 patients with chronic mitral regurgitation. When compared with normal subjects, patients with chronic aortic and mitral regurgitation had similarly dilated and hypertrophied left ventricles (p less than 0.0005), while only mitral regurgitation patients had significantly enlarged (p less than 0.0005) mean left atrial dimension and volume. Likewise, plasma atrial natriuretic factor was elevated among patients with mitral regurgitation (60.3 +/- 47.0 fmol/ml) but was normal in patients with aortic regurgitation (19.0 +/- 11.0 fmol/ml versus 12.4 +/- 5.2 fmol/ml in normals; both p less than 0.0005 versus mitral regurgitation). Among all 97 subjects, atrial natriuretic factor levels correlated more closely with left atrial dimension and volume (r = 0.62 and 0.64, p less than 0.0005) than with left ventricular dimension (r = 0.44, p less than 0.0005) or mass (r = 0.40, p less than 0.0005). In addition, multivariate analysis indicated that left atrial volume bore a stronger independent relationship to plasma atrial natriuretic factor levels than either age or left ventricular variables.(ABSTRACT TRUNCATED AT 250 WORDS)     

Mechanism of altered pattern of left ventricular filling with aging in subjects without cardiac disease

The mechanism whereby aging, in the absence of cardiac disease, may alter the pattern of left ventricular (LV) diastolic filling is unknown. Accordingly, this study was designed to examine the factors that may be in part responsible for aging's effect on the pattern of LV diastolic filling. The LV end-diastolic pressure-volume relation was analyzed in 11 elderly subjects (68 +/- 5 years, mean +/- standard deviation) and 15 normal young adults (31 +/- 7 years) without coronary artery disease, systemic hypertension, LV hypertrophy or abnormality of LV systolic function. After catheterization, the subjects underwent pulsed Doppler analysis of mitral flow. All had normal 2-dimensional echocardiograms without LV or valvular dysfunction. Peak early filling velocity in the elderly subjects was decreased in comparison with that in young adults (61 +/- 14 vs 83 +/- 8 cm/s, p less than 0.001) and the ratio of early and late diastolic filling velocity was reduced (0.81 +/- 0.26 vs 1.88 +/- 0.40, p less than 0.001). The isovolumic relaxation time did not differ between the elderly and young subjects (158 +/- 20 vs 146 +/- 22 ms, difference not significant). In the elderly, LV end-diastolic pressure was increased (15 +/- 7 vs 11 +/- 4 mm Hg, p less than 0.05) despite a smaller end-diastolic volume index (60 +/- 16 vs 74 +/- 18 ml/m2, p less than 0.05), indicating a shift of the passive diastolic pressure-volume relation. It was concluded that early diastolic filling is reduced in normal aged subjects, even in the absence of coronary artery disease and systolic dysfunction. This altered pattern of diastolic filling may result from a shift of the passive LV diastolic pressure-volume relation.     

Coronary arterial remodeling studied by high-frequency epicardial echocardiography: an early compensatory mechanism in patients with obstructive coronary atherosclerosis

Coronary arterial remodeling is a compensatory mechanism that may limit the adverse effects of coronary obstructive lesions by expansion of the entire vascular segment. To determine if this compensatory anatomic change occurs in patients, high-frequency epicardial echocardiography using a 12 MHz transducer was performed during open heart surgery in 33 patients (10 with normal coronary arteries undergoing valvular surgery and 23 with coronary atherosclerosis). From stop-frame videotape high-frequency epicardial echocardiographic images, cross-sectional measurements of luminal area and total arterial area (lumen, intima, media and dense adventitia) were made in the patients with atherosclerosis at the site of arterial lesions and from the most proximal portion of the same artery. Remodeling was defined as enlargement of the total arterial area. In normal arteries measurements were made from proximal and midarterial locations. In the patients with normal coronary arteries, total arterial area, as determined by high-frequency echocardiography, decreased from the proximal site to the midportion of the artery (from 10.4 +/- 0.9 to 8.4 +/- 1.0 mm2, p less than 0.05); luminal area also decreased (from 6.0 +/- 0.6 to 4.5 +/- 0.7 mm2, p less than 0.05). In patients with coronary arterial lesions, luminal area also decreased from the proximal site to the arterial lesion site (from 5.3 +/- 0.6 to 2.3 +/- 0.3 mm2, p less than 0.05), but total arterial area increased (from 11.6 +/- 1.0 to 13.0 +/- 1.0 mm2, p less than 0.05). Of the 25 coronary arteries evaluated, only 4 had angiographic evidence of coronary collateral formation. These data indicate that coronary arterial remodeling is an important compensatory mechanism in obstructive coronary disease.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of H1-receptor stimulation on coronary arterial diameter and coronary hemodynamics in humans

Effects of H1-receptor stimulation on coronary arterial diameter and coronary hemodynamics were examined in 11 patients with angiographically normal coronary arteries and without variant angina or resting angina. Selective H1-receptor stimulation was achieved by infusing histamine into the left coronary artery at a rate of 2.0 micrograms/min for 5 minutes after pretreatment with cimetidine (25 mg/kg). Plasma histamine concentration in the coronary sinus, coronary sinus blood flow, heart rate, and aortic pressure were measured before, during, and after the histamine infusion. Coronary arterial diameter was measured by cinevideodensitometric analysis of coronary arteriograms performed before and immediately after the histamine infusion. During the histamine infusion, plasma histamine concentration in the coronary sinus increased from 0.33 +/- 0.06 to 5.86 +/- 0.71 ng/ml (p less than 0.01); coronary sinus blood flow increased from 98 +/- 12 to 124 +/- 13 ml/min (p less than 0.01), and coronary vascular resistance decreased from 1,113 +/- 117 to 851 +/- 91 mm Hg.min/l (p less than 0.01). Heart rate and aortic pressure remained unchanged. The mean luminal diameters of the proximal, middle, and distal left anterior descending artery increased by 9.4 +/- 3.6% (p less than 0.05), 19.2 +/- 3.8% (p less than 0.001), and 31.5 +/- 5.6% (p less than 0.001), respectively, after the histamine infusion. The mean luminal diameters of the proximal, middle, and distal left circumflex artery increased by 15.2 +/- 3.6% (p less than 0.01), 17.5 +/- 5.2% (p less than 0.01), and 20.6 +/- 4.3% (p less than 0.001), respectively, after the histamine infusion.(ABSTRACT TRUNCATED AT 250 WORDS)     

Impact of valvular regurgitation on left ventricular geometry and function in hypertensive patients with left ventricular hypertrophy: the LIFE study

Mild-to-moderate aortic and mitral regurgitation are frequently detected by echocardiogram in asymptomatic hypertensive patients. Our goal was to assess the prevalence and impact of mild-to-moderate mitral and/or aortic regurgitation on left ventricular (LV) structure and function in patients with hypertension and LV hypertrophy (LVH). Hypertensive patients with ECG LVH enrolled in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) echocardiography substudy were evaluated. Among 939 patients with needed LV measurements and Doppler data, 242 had mild (1+) valvular regurgitation, and 51 patients had moderate (2+ or 3+) regurgitation of one or both valves. In analyses adjusting for gender, patients with mild mitral and/or aortic regurgitation had larger LV internal dimensions (5.25 vs 5.33 cm, P<0.05), higher LV mass indexed for body surface area (122 vs 125 g/m(2), P<0.05) or height(2.7) (55.4 vs 57.3, P<0.05), and larger left atrial diameter. Patients with moderate regurgitation of one or both valves had larger LV chambers (5.25 vs 5.9 cm, P<0.001), greater mean LV mass (232 vs 248 g, P<0.001) and LV mass indexed for body surface area or height(2.7), and higher Doppler stroke volume. Patients with moderate valvular regurgitation also had a higher prevalence of LVH due to an increased prevalence of eccentric LVH. There were no differences among groups defined by the presence and severity of valvular regurgitation in cardiac output, total peripheral resistance, or pulse pressure/stroke volume, indicating that the observed inter-group differences in LV geometry were not due to differences in the haemodynamic severity of hypertension. Hypertensive patients with mild-to-moderate mitral or aortic valvular insufficiency have additional LV structural and functional changes that may affect prognosis.     

Coronary circulation in asymmetrical hypertrophy of the interventricular septum. On a new pathogenic hypothesis

Thirty-four patients with left ventricular hypertrophy were studied. In all cases the following parameters were analyzed: 1) Echocardiography:left ventricular diastolic and systolic diameters, ejection fraction, thickness and movement of interventricular septum and posterior wall of the left ventricle (LV) 2) Electrocardiography: R wave voltaje in precordial leads V2, V3 and V5 and electrical axis in frontal plane 3) Catheterization: intracavitary pressures in LV and aortic pressures 4) Left ventriculography: areas of altered contractility 5) Coronariography: distribution pattern of coronary arteries and number of first order branches of circumflex (CA) and anterior descending coronary arteries (ADCA). The population was divided into 2 groups. Group A (GA) was made up of 22 patients with concentric hypertrophy (CH) of the LV (15 with systemic hypertensive heart disease, 6 with aortic valvular stenosis and 1 idiopathic). Echocardiographic findings included posterior wall thickness (PWT) or septal thickness of 1.1. cm or more and interventricular septum-posterior wall thickness ratio (S/PW) of less than 1.3. Group B (GB) included 12 patients with asymmetric septal hypertrophy (ASH), idiopathic in 5, systemic hypertensive heart disease in 4 and aortic valvular stenosis in 3. In these patients the S/PW thickness ratio was greater than 1.3 and the thickness of either wall greater than 1.1. cm. When the data of the two groups were compared there were significant differences in relation to the presence of septal hypertrophy. The R wave voltage in V2, interventricular thickness and S/PW were greater in GB. In addition, septal movement was less in GB than in Group A (0.47 +/- 0.26 cm vs. 0.74 +/- 0.37 cm; P less than 0.05). PWT was also less in Group B than in A (B: 1.01 +/- 0.1 cm, A: 1.2 +/- 0.2 cm; P less than 0.001). The CA in Group B divided into fewer than 4 first order branches to the upper two thirds of the posterior and lateral walls of the LV in 91.6%. This distribution of circumflex branches was found in 31.8% of the patients in Group A (P less than 0.05). In Group B, the ADCA divided into septal branches with no more than 2 diagonal branches. The posterior descending artery dominated septal distribution in 100% of these cases (GA: 31.8%; P less than 0.05). The sum of the first order branches of the CA and the ADCA was 5.6 +/- 0.9 in Group A and 2.7 +/- 0.9 branches in Group B (P less than 0.01).(ABSTRACT TRUNCATED AT 400 WORDS)     

Anatomo-functional correlations of changes in electrocardiographic repolarization in aortic and mitral valve insufficiency. Comparison of indices based on QRS voltages

Electrocardiographic repolarization changes and voltage criteria for left ventricular hypertrophy were examined, in relation to hemodynamic, echocardiographic and angiographic data. This was done to evaluate their association with abnormalities in cardiac function and structure in 53 patients with chronic aortic regurgitation and 36 patients with chronic mitral regurgitation. No patient showed evidence of coronary artery disease. Of the patients with aortic regurgitation, the 27 patients with an abnormal repolarization pattern at ECG had worse NYHA functional class when compared to the 24 patients with normal repolarization (2.4 +/- 1 vs 1.6 +/- 0.9; p less than .01). They also had greater left ventricular dimensions (end-diastolic volume: 162 +/- 57 ml/m2 vs 109 +/- 15 ml/m2, p less than .01; end-systolic volume: 85 +/- 46 ml/m2 vs 44 +/- 31 ml/m2, p less than .01), lower left ventricular ejection fraction (.50 +/- .12 vs .63 +/- .14; p less than .01), greater left ventricular mass (170 +/- 56 gr/m2 vs 119 +/- 29 gr/m2; p less than .01) and higher end-diastolic left ventricular pressure (21 +/- 11 mmHg vs 11 +/- 8 mmHg; p less than .01). QRS voltage was less closely related to cardiac function and structure and thus, did not modify the conclusions based on repolarization findings alone. Furthermore, repolarization patterns identified patient subgroups with high or low prevalences of previously described predictors of poor surgical outcome. The presence or absence of the "strain" pattern was not related to differences in cardiac structure and function, in patients with mitral regurgitation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Aortic distensibility abnormalities in coronary artery disease

Vasodilatory capacity of nonstenotic arteries in experimental animals with atherosclerosis is decreased. It was postulated that aortic distensibility may be abnormal in patients with coronary artery disease (CAD). Aortic distensibility was determined in 24 normotensive patients with CAD and an angiographically normal aorta and values were compared with those in 18 age-matched normal subjects. Aortic diameters were measured at 3 levels--2, 4 and 6 cm above the aortic valve--by angiographic techniques. The area of the first 6 cm of the aorta above the aortic valve was planimetered and mean aortic diameters were calculated. Distensibility was calculated using the formula: [2 X (changes of the aortic diameter)/(diastolic aortic diameter) X (changes of the aortic pressure)]. CAD patients had similar aortic pressures but markedly lower distensibility than normal subjects: 0.7 +/- 0.2 vs 1.7 +/- 0.3 (p less than 0.02); 1.5 +/- 0.3 vs 4.0 +/- 0.6 (p less than 0.02); and 1.2 +/- 0.2 vs 5.3 +/- 0.6 (p less than 0.001) at 2, 4 and 6 cm above the aortic valve, respectively. Distensibility was also calculated from the mean aortic diameters and was greater in normal subjects than in CAD patients (3.4 +/- 0.4 vs 1.6 +/- 0.1, p less than 0.001). Decreased aortic distensibility in CAD may be related to the common atherosclerotic process or to reduced ascending aorta vasa vasorum flow from coronary arteries.     

Factors influencing left ventricular structure and stress-corrected systolic function in men and women with asymptomatic aortic valve stenosis (a SEAS Substudy)

To identify determinants of left ventricular (LV) structure and stress-corrected systolic function in men and women with asymptomatic aortic stenosis (AS), Doppler echocardiography was performed at baseline in 1,046 men and 674 women 28 to 86 years of age (mean 67 +/- 10) recruited in the Simvastatin Ezetimibe in Aortic Stenosis (SEAS) study evaluating placebo-controlled combined simvastatin and ezetimibe treatment in AS. LV hypertrophy was less prevalent in women despite older age, higher systolic blood pressure, and smaller aortic valve area/body surface area (all p values <0.05). In logistic regression analyses, LV hypertrophy was independently associated with male gender, severity of AS, hypertension, higher systolic blood pressure, and lower stress-corrected midwall shortening (scMWS) or stress-corrected fractional shortening (scFS; all p values <0.01). In men aortic regurgitation also was a predictor of LV hypertrophy (p <0.05). Women had greater scFS and scMWS when corrected for LV size or geometry (all p values <0.001). In multivariate analyses, female gender predicted 11% greater scFS and 4% greater scMWS independent of age, body mass index, heart rate, aortic valve area, LV mass, relative wall thickness, aortic regurgitation, hypertension, and end-systolic stress (R(2) = 0.23 and 0.59, respectively, p <0.001). In conclusion, the major determinants of LV hypertrophy in patients with asymptomatic AS are male gender, severity of AS, and concomitant hypertension. Women have higher stress-corrected indexes of systolic function independent of LV geometry or size, wall stress, older age, or more concomitant hypertension.