Concentric left ventricular hypertrophy in patients with aortic regurgitation

Chronic aortic regurgitation (AR) is a disease incorporating volume overload of the left ventricle (LV) which is characterized by hyperactive left ventricular dilatation (LVD). However, we have encountered several patients who had concentric LV hypertrophy (LVH) instead of LVD. We therefore studied 50 consecutive patients with isolated AR but without aortic stenosis and found seven patients with concentric LVH having LV wall thickness (determined by summing ventricular septal and posterior wall thicknesses) exceeding 30 mm and LV diastolic diameters of less than 60 mm. These seven patients with AR and LVH were older (55 +/- 27 vs 42 +/- 11 years) and tended to have milder degree of AR, compared with the remaining 43 patients having AR and LVD. However, patients with AR and LVH did not differ from AR and LVD as to the cardiothoracic ratio, SV1 + RV5, T-waves, ejection fraction, operative findings of valvular morphology and underlying etiologies. In contrast, patients with AR and LVH presented higher systolic (196 +/- 41 vs 149 +/- 26 mmHg, p less than 0.01) and diastolic pressures (74 +/- 14 vs 51 +/- 13 mmHg, p less than 0.01) and higher systemic vascular resistance (1,854 +/- 399 vs 1,388 +/- 352 dyne.sec.cm-5, p less than 0.05) during catheterization than did those with AR and LVD. However, blood pressure at the time of admission was not different in the two groups. These observations indicate that concentric LVH is not rare among patients with AR, and that an association of pressure overload with volume overload of the LV, particularly during exercise or stress, may lead to concentric LVH, even in patients with chronic AR.     

Evaluation of left ventricular performance in aortic stenosis, aortic regurgitation and mitral regurgitation from the stroke work/left ventricular mass ratio.

Evaluation of left ventricular performance in aortic stenosis, aortic regurgitation and mitral regurgitation from the stroke work/left ventricular mass ratio. Europ. J. Cardiol., 10/4, 279--294. 132 patients with a pure valvular dysfunction affecting a single orifice, namely aortic stenosis, aortic or mitral regurgitation, were studied. All patients, including 20 control subjects, underwent hemodynamic examination of both right and left heart chambers including left cineangiography. Using the stroke work index/myocardial mass ratio (SWI/MLV), for which the limits in normal subjects are narrow (0.81 +/- 0.03 . g-1) it was possible to divide these patients into three groups: Group I (SWI/MLV greater than 0.87 gm . g-1) characterized by a proportionately greater increase in stroke work index than myocardial mass (hyperfunctioning ventricle). Group II (0.87 gm . g-1 greater than or equal to SWI/MLV greater than or equal to 0.75 gm . g-1) characterized by a parallel increase in stroke work index and myocardial mass (normally functioning ventricle). Group III (SWI/MLV less than 0.75 gm . g-1) for which the increase in myocardial mass was proportionately greater than that of the stroke work index (hypofunctioning ventricle). As one progresses from group I to III, there is a concomitant fall in ventricular function with decreased mean velocity of circumferential fiber shortening (VCF), ejection fraction (EF) and increased enddiastolic volume (EDV) together with the hypertrophy of the left ventricle during the last stage. We conclude that the SWI/MLV ratio is an easy to calculate index, independent of the unerlying dysfunction, which evaluates left ventricular function by taking into account the myocardial mass.     

Disparate impact of severe aortic and mitral regurgitation on left ventricular dilation

In asymptomatic severe aortic (AR) and mitral regurgitation (MR), left ventricular (LV) dimension criteria were established to guide timing of valve replacement to prevent irreversible LV dysfunction. Given both lesions are primary LV volume overload ''leaks'', it might be expected that both lesions would induce similar impact on the LV and result in equivalent dimension criteria for intervention. However, the dimension-based intervention criteria for AR versus MR (developed through natural history studies), differ markedly. The pathophysiological foundations for such discordance have neither been fully elucidated nor emphasized. This case-based treatise compares the two regurgitant lesions with respect to: (a) ''total regurgitant circuits''; (b) ''driving pressures'' resulting in LV volume overload from each respective ''leak''; and (c) volume and afterload wall stresses imposed on the LV. Key points

• The ''total circuits'' of volume overload differ: The AR circuit includes the LV and systemic vasculature, whereas MR includes the LV ejecting into the left atrium/pulmonary veins and systemic circulation.
• The ''driving pressure'' of regurgitation and afterload are high with AR and low with MR.
• Differing ''total circuits'' and ''driving pressures'' impose disparate wall stresses upon the LV. Parallel and serial sarcomere replication occurs in AR, while only serial replication occurs in MR.

It therefore follows that for regurgitation of similar severities, AR results in greater LV dilation at the point of irreversible myocardial dysfunction compared to MR. These considerations may explain, at least in part, the disparate dimension criteria employed for valve intervention for severe AR vs MR.     

Vectorcardiographic comparison of left ventricular hypertrophy in idiopathic hypertrophic subaortic stenosis, aortic stenosis, and aortic regurgitation

Frank vectorcardiograms in 21 patients with idiopathic hypertrophic subaortic stenosis and asymmetric septal hypertrophy (IHSS), 25 patients with severe aortic valve stenosis (AS), and 20 patients with severe aortic regurgitation (AR) were analyzed. Patients with mixed valvular lesions, pulmonary hypertension, coronary artery disease, or QRS width ≥ 0.12 sec. were excluded. The QRS loops were analyzed at 10 msec. intervals (0.01 to 0.07 sec.), and mean spatial vectors were derived. Spatial magnitude, azimuth, and elevation were measured. The magnitudes of the 0.01 and 0.02 sec. vectors were significantly larger in AR than in AS (p < 0.01 and p < 0.05, respectively). The magnitude of the midloop vectors (0.04 sec.) was largest in AS (p < 0.02) while the 0.05 sec. vector was largest in AR (p < 0.01). No significant differences in azimuth, elevation, time of maximal spatial vector, or QRS duration were noted among the three groups. Only two of 21 patients with IHSS demonstrated the pattern of pseudo-infarction. In the remaining patients, the analyzed vectors failed to distinguish the asymmetric septal hypertrophy of IHSS from the concentric hypertrophy of AS.     

Presystolic mitral closure sound in aortic regurgitation with left ventricular hypertrophy and first degree heart block

We report a patient who developed aortic regurgitation and first degree atrioventricular block caused by infective endocarditis complicating aortic valve stenosis. There was premature closure of the mitral valve and, in the absence of an Austin Flint murmur, a simultaneous high frequency sound was audible which we regard as a presystolic first heart sound. That such a sound may be associated with valve closure, even though this precedes electrical and mechanical ventricular systole, provides further support for the valvular origin of the first heart sound.     

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)     

Presystolic mitral closure sound in aortic regurgitation with left ventricular hypertrophy and first degree heart block.

We report a patient who developed aortic regurgitation and first degree atrioventricular block caused by infective endocarditis complicating aortic valve stenosis. There was premature closure of the mitral valve and, in the absence of an Austin Flint murmur, a simultaneous high frequency sound was audible which we regard as a presystolic first heart sound. That such a sound may be associated with valve closure, even though this precedes electrical and mechanical ventricular systole, provides further support for the valvular origin of the first heart sound.     

Left ventricular performance following mitral valve replacement in patients with tight mitral stenosis combined with mild aortic regurgitation

The severity of aortic regurgitation is difficult to estimate prior to mitral valve replacement (MVR) in cases with tight mitral stenosis (MS), because low output state due to mitral obstruction masks signs of aortic regurgitation. This study clarified left ventricular performance, possibly affected by increased diastolic loading after MVR. The study subjects consisted of 12 patients with pure mitral stenosis (MS group) and 11 with combined mitral stenosis and aortic regurgitation (MSAR group). The diagnosis was made by cardiac catheterization preoperatively. The aortographic grade of aortic regurgitation was class 1 or 2 according to the AHA classification. Both groups were matched in terms of severity in mitral obstruction evaluated by mitral valve area. On preoperative echocardiographic evaluation, there was no difference in the mean values of LVDd, LVSd, and %FS between the groups MS and MSAR. After surgery, symptoms improved in each patient. Echocardiography performed three months after MVR revealed no differences in these parameters between both the groups. We concluded that aortic regurgitation evaluated as class 1 or 2 preoperatively does not increase in respect to left ventricular diastolic overloading and echocardiographic left ventricular performance remains unchanged.     

Preoperative left and right ventricular performance in combined aortic and mitral regurgitation and comparison with isolated aortic or mitral regurgitation

Left and right ventricular performance characteristics in operative candidates with combined aortic and mitral regurgitation (AR/MR) have not been well defined. Therefore, we determined radionuclide cineangiographic ejection fractions, as well as echocardiographic and hemodynamic parameters, in 8 symptomatic patients undergoing double-valve replacement with pure, severe AR/MR. In order to gain insight into the basis for the poor postoperative survival in patients with this intrinsically biventricular disease, we compared these results with those of 29 symptomatic patients with isolated AR and with 18 symptomatic patients with isolated MR, all also undergoing valve replacement. Before operation, patients with AR/MR had significantly lower left ventricular (LV) ejection fraction than patients with MR (rest, 40 +/- 9% vs 52 +/- 10%, p less than 0.025; exercise, 35 +/- 12% vs 54 +/- 12%, p less than 0.005) and tended to have lower LV ejection fraction than patients with AR alone (rest, 40 +/- 9% vs 45 +/- 12%, difference not significant; exercise, 35 +/- 12% vs 39 +/- 11%, difference not significant); right ventricular (RV) ejection fraction was lower in AR/MR than in AR (p less than 0.01), and tended to be lower than in MR (difference not significant). At average postoperative follow-up of 72 to 76 months (survivors in each group), symptomatic patients with AR/MR had significantly poorer survival than symptomatic patients with isolated MR (p less than 0.05) and were more likely to have persistent symptoms than patients with AR (p less than 0.05). These findings suggest that symptomatic patients with AR/MR have poorer LV and RV performance than similarly symptomatic operative candidates with AR or MR alone.(ABSTRACT TRUNCATED AT 250 WORDS)     

Diastolic left ventricular pressure-volume and stress-strain relations in patients with valvular aortic stenosis and left ventricular hypertrophy.

Left ventricular (LV) chamber and myocardial stiffness were determined in 17 patients, four subjects with normal LV function and 13 subjects with valvular aortic stenosis and concentric myocardial hypertrophy, using simultaneous catheter micromanometry and LV cineangiography. Pressure (P), volume (V), and wall thickness (h) were measured. Variability in both chamber and myocardial stiffness parameters was found with five of the aortic stenosis patients (Group 1, left ventricular end-diastolic pressure = 15 +/- 2 (SEM) mm Hg) exhibiting normal values for end-diastolic dP/dV and dP/dV/V, for chamber stiffness constants (a,a') derived from P-V and normalized P-V relations, respectively, for end-diastolic myocardial elastic stiffness (ES or EE, where S = spherical model and E = ellipsoidal model) at the midwall of the minor axis circumference, and for the myocardial stiffness constants (KS or KE) of the circumferential stress-strain relation. Eight other patients with aortic stenosis (Group II, left ventricular end-diastolic pressure = 20 +/- 3 (SEM) mm Hg) exhibited significant increases in end-diastolic dP/dV,dP/dV/V,ES and EE and a tendency for increase in the chamber stiffness constants (a,a') and myocardial stiffness constants (KS, KE). These observations suggest that concentric increase in muscle mass (increase in wall thickness/minor axis radius ratio and wall volume/chamber volume ratio) is an important determinant of elevated mid- and late diastolic pressures in patients with valvular aortic stenosis, while concurrently mitigating increases in both systolic and diastolic wall stress. In some patients with aortic stenosis, however, diastolic filling pressures are elevated more severely, not only as a result of concentric hypertrophy, but also in response to augmented muscle stiffness. Reversibility of increased ventricular diastolic stiffness and elevated filling pressures was documented as concentric hypertrophy regressed post-aortic valve replacement in one patient, suggesting that fibrosis is not invariably the cause of enhanced myocardial stiffness in this secondary and compensatory form of hypertrophy.     

Prognostic implications of left ventricular function during exercise in asymptomatic patients with aortic regurgitation

Few data are available that address the prognostic implications of the response of the left ventricle (LV) to exercise in asymptomatic patients with aortic regurgitation (AR) who have normal resting LV function. Thirty-one such patients were contacted two to seven years after rest and exercise radionuclide ventriculography. Eleven had had significant cardiovascular events. Event-free survival at forty-eight months was 64%. Ten of eleven events occurred in 21 patients with decline in ejection fraction (EF), but the magnitude of decline did not further separate the group with regard to prognosis. Eight events (73% of total events) occurred in the 11 patients (35% of total patients) with an EF during exercise of 0.55 or less. The short and intermediate outlook for asymptomatic patients with AR and normal resting LV function is good regardless of the response of the EF to exercise, but an exercise EF less than or equal to 0.55 does identify a relatively high-risk subset for deterioration beyond twenty-four months.     

Mechanisms and clinical implications of asymptomatic mitral regurgitation in patients with left ventricular dysfunction.

BACKGROUND: Functional mitral regurgitation (MR) is common in patients with chronic heart failure (CHF). During exercise, hemodynamic changes such as elevation of blood pressure and an increase in the left ventricular end-diastolic dimension may increase MR. Severity of CHF is reflected by exercise tolerance and, therefore, MR during exercise is supposed to indicate the severity of heart failure. The degree of MR increase and left ventricle (LV) shape was quantified during exercise in CHF patients and were compared with exercise tolerance. METHODS AND RESULTS: Twenty patients with CHF (mean age: 63 years) underwent dynamic cycle exercise at steady-state levels of 80% and 150% of the anaerobic threshold (AT). The MR jet area and left atrial (LA) area were measured during exercise and the ratio of MR/LA was calculated. The LV shape was assessed by calculating the ratio of the major to the minor axis. The MR/LA ratio increased during exercise (rest: 16.9+/-6.5%, 80% AT: 21.9+/-8.9%, 150% AT: 30.9+/-11.2%; p<0.01) and the LV shape became more spherical (rest: 1.34+/-0.10, 80% AT: 1.31+/-0.10, 150% AT: 1.23+/-0.11; p<0.05). There was a negative correlation between MR/LA ratio and the ratio of the major to the minor axis (-0.722, r<0.01). CONCLUSIONS: MR during exercise increases as the severity of CHF increases. Functional MR is correlated with the shape of the LV.     

Gender differences in factors influencing electrocardiographic findings of left ventricular hypertrophy in severe aortic stenosis

We investigated gender differences in factors influencing the electrocardiographic (ECG) findings of left ventricular hypertrophy (LVH) in patients with severe aortic stenosis (AS). The functional and geometric responses of the left ventricle to chronic pressure overload, such as hypertension and AS, have been reported to be different between men and women. However, gender differences in the factors influencing the ECG findings of LVH in pressure overload remain unknown. We conducted a retrospective observational study in consecutive patients with severe AS (aortic valve area (AVA) assessed by cardiac catheterization <1.0 cm²) without concomitant significant aortic regurgitation, mitral stenosis and/or regurgitation, conduction disturbance, or myocardial infarction (n = 35 males, 68 females). The ECG criteria were classified into three categories: (1) high voltage by the Sokolow–Lyon index associated with ST-T wave changes (with no digitalis therapy); (2) high voltage alone; and (3) normal. Groups 1 and 2 were defined as LVH on ECG. We compared the ECG findings in relation to the AS severity between genders. Women were older, but there were no significant differences in the prevalence of hypertension, AVA index (AVAI), mean pressure gradient or peak velocity across the AV, LV mass index (LVMI) derived from echocardiography or the distribution of ECG categories between genders. A multiple logistic regression analysis including age, gender, hypertension, AVAI, mean pressure gradient, and LVMI revealed that the LVMI (P = 0.001) and AVAI (P = 0.0434) were significantly related to the distribution of ECG categories. LVMI significantly predicted LVH on ECG in both genders, but AVAI was a predictive factor in only women. ECG LVH in patients with severe AS may be mainly reflected by LVMI in men and by both LVMI and AVAI in women. Factors other than AVA, such as end-stage disease and/or complicating factors such as hypertension, may underlie the observed differences in ECG findings of LVH between men and women.     

Mitral valve replacement in patients with severe mitral regurgitation and impaired left ventricular function.

We have studied short- and mid-term effects of preservation and excision of the mitral subvalvar support during mitral valve replacement in 40 patients, who had developed moderate to severe degree of left ventricular function impairment, secondary to pure severe mitral regurgitation. These patients had valve replacement, because valve anatomy was unsuitable for reconstructive procedures. Mitral subvalvar support was excised and valve replaced with a Bj?rk-Shiley prosthesis, in 10 patients with moderately impaired left ventricular ejection fraction (mean 32% +/- 1.2%) and in 18 patients with severely impaired left ventricular function (left ventricular ejection fraction: 22% +/- 0.8%). In 12 patients with severely impaired left ventricular function (left ventricular ejection fraction: 20% +/- 1%) posterior subvalvar apparatus was preserved and valve replaced with a bioprosthesis. Prognosis of patients with moderately impaired left ventricular function was not influenced by the loss of chordopapillary support. Actuarial survival at 8 and 10 years was 46% +/- 7.8% for patients with severely impaired left ventricular function with chordopapillary support excised and 70% +/- 10% for patients with severely impaired left ventricular function with chordopapillary support preserved (p less than 0.01). Preservation of mitral subvalvar support is important in patients with severely impaired left ventricular function (left ventricular ejection fraction less than 25%).