Ventricular arrhythmias in aortic valve disease before and after aortic valve replacement.

In order to evaluate the effect of aortic valve replacement on the incidence of ventricular arrhythmias in patients with aortic valve disease, 24-hour ambulatory electrocardiographic recordings were obtained before surgery in 96 patients without coronary artery disease (aortic stenosis n = 50, combined aortic stenosis and regurgitation n = 19 and aortic regurgitation n = 27). Following aortic valve replacement, repeat recordings were obtained after 13 +/- 4 days and 18 +/- 7 months. Ventricular arrhythmias were in all cases classified according to Lown and were compared with clinical, echocardiographic and hemodynamic data. Preoperatively, ventricular premature beats were observed in 85 patients (89%) and were frequent (greater than 30 ventricular premature beats/hour) in 20 (21%). Multiformity was found in 27 (28%), couplets in 18 (19%) and ventricular tachycardia in 11 (11.5%). The occurrence of ventricular arrhythmias was not related to the type or severity of valve lesions. Patients with severe ventricular arrhythmias (Lown class 3 or 4: 37%) had a greater thickness of their interventricular septum 13.9 +/- 2.5 mm, vs 11.7 +/- 2.6 (p less than 0.05); a higher LV mass 176 +/- 34 g/m2, vs 134 +/- 39 (p less than 0.05) and a lower left ventricular ejection fraction 47 +/- 12%, vs 57 +/- 11, (p less than 0.01). Two weeks postoperatively, the incidence and severity of ventricular arrhythmias had increased: ventricular premature beats were noted in 92% and were severe in 50%. No correlation was found between ventricular arrhythmias and preoperative or operative data. Eighteen months after surgery, ventricular premature beats were still observed in 81% of patients but remained frequent in 7% only. Severe ventricular arrhythmias were noted in 27%. Patients with severe ventricular arrhythmias had at the time of this late recording a lower radionuclide left ventricular ejection fraction 57 +/- 14%, vs 73 +/- 9 (p less than 0.02) and a higher enddiastolic diameter 63 +/- 15 mm, vs 48 +/- 7, (p less than 0.01). This study indicates that ventricular arrhythmias are common in patients with aortic valve disease. The severity of arrhythmias is influenced by the LV consequences of valve lesion both pre- and late postoperatively. The frequency and severity of ventricular arrhythmias increase early after surgery and do not correlate with preoperative or operative data.     

Ventricular arrhythmias in patients with aortic valve disease (author's transl)

In order to investigate the incidence of severe ventricular arrhythmias, the 24-h ambulatory ECG of 55 patients with aortic valve disease (NYHA classes I-IV; stenosis: n = 24; regurgitation: n = 18; mixed lesions: n = 13) without coronary heart disease were evaluated with regard to the number of premature ventricular beats and according to the Lown classification. Ventricular arrhythmias were found in 73% of all patients (Lown classes III-V: 38%; Lown classes IV-V: 20%). A significant relation between the degree of arrhythmias and the gradient or severity of regurgitation of the aortic valve could not be established. However, there was a significant linear correlation between the left ventricular ejection fraction and the degree of arrhythmias (stenosis: r = 0.60; regurgitation: r = -0.72; mixed lesions: r = 0.78; all p less than 0.005). Complex arrhythmias of Lown classes III-IV are rare (less than 10%) in patients with good left ventricular function (LVEF greater than 60%). There was a history of palpitations in 81% of patients with Lown classes III-V. According to these data, ventricular arrhythmias are present in a large number of patients with aortic valve disease. The degree of arrhythmia does not correlate to the transvalvular stenosis or the severity of regurgitation, but is strongly influenced by the myocardial performance. Therefore in patients with aortic valve disease significant arrhythmias are frequently a sign of impaired LV function.     

Reduced aortic elasticity and dilatation are associated with aortic regurgitation and left ventricular hypertrophy in nonstenotic bicuspid aortic valve patients.

OBJECTIVES: This study sought to assess elasticity and dimensions of the aorta and their impact on aortic valve competence and left ventricular (LV) function in patients with a nonstenotic bicuspid aortic valve (BAV). BACKGROUND: Intrinsic pathology of the aortic wall is a possible explanation for reduced aortic elasticity and aortic dilatation in patients with BAVs, even in the absence of a stenotic aortic valve. The relationship between aortic wall elasticity, aortic dimensions, aortic valve competence, and LV function in patients with BAVs has not previously been studied with magnetic resonance imaging. METHODS: Magnetic resonance imaging was performed in 20 patients with nonstenotic BAVs (mean +/- SD, age 27 +/- 11 years) and 20 matched control patients. RESULTS: The BAV patients showed reduced aortic elasticity as indicated by increased pulse wave velocity in the aortic arch and descending aorta (5.6 +/- 1.3 m/s vs. 4.5 +/- 1.1 m/s, p = 0.01; and 5.2 +/- 1.8 m/s vs. 4.3 +/- 0.9 m/s, p = 0.03, respectively), and reduced aortic root distensibility (3.1 +/- 1.2 x 10(-3) mm Hg(-1) vs. 5.6 +/- 3.2 x 10(-3) mm Hg(-1), p < 0.01). In addition, BAV patients showed aortic root dilatation as compared with control patients (mean difference 3.6 to 4.2 mm, p < or = 0.04 at all 4 predefined levels). Minor degrees of aortic regurgitation (AR) were present in 11 patients (AR fraction 6 +/- 8% vs. 1 +/- 1%, p < 0.01). The LV ejection fraction was normal (55 +/- 8% vs. 56 +/- 6%, p = 0.61), whereas LV mass was significantly increased in patients (54 +/- 12 g/m2 vs. 46 +/- 12 g/m2, p = 0.04). Dilatation at the level of the aortic annulus (r = 0.45, p = 0.044) and reduced aortic root distensibility (r = 0.37, p = 0.041) correlated with AR fraction. Increased pulse wave velocity in the aortic arch correlated with increased LV mass (r = 0.42, p = 0.041). CONCLUSIONS: Reduced aortic elasticity and aortic root dilatation were frequently present in patients with nonstenotic BAVs. In addition, reduced aortic wall elasticity was associated with severity of AR and LV hypertrophy.     

Low dose dobutamine echocardiography in the assessment of contractile reserve to predict the outcome of valve replacement for chronic aortic regurgitation

BACKGROUND: When to perform surgery for aortic regurgitation is a difficult clinical decision. Occult left ventricular (LV) dysfunction may be present in patients with minimal or no symptoms, and in some patients LV dysfunction may persist after valvular replacement. OBJECTIVES: To examine the role of preoperative low dose dobutamine echocardiography (LDDE) in predicting postoperative outcome in patients who had aortic valve replacement for aortic regurgitation. PATIENTS AND METHODS: The study group comprised 16 patients (15 men, aged 48 +/- 15 years) undergoing elective surgery for aortic regurgitation. Preoperative echocardiograms were obtained in the resting state and during dobutamine infusion at 7.5 micrograms/kg/min. Complete recovery was defined by normalization of LV size and function, and the absence of symptoms at the six-month follow-up visit. Patients with complete recovery (group 1) and without complete recovery (group 2) were compared in relation to their echocardiographic parameters at rest and during LDDE. RESULTS: Of 16 patients in the study, nine were in group 1 and seven were in group 2. Age, functional class and LV end-diastolic dimensions were similar between the two groups. Group 1 patients had a smaller preoperative LV end-systolic dimension index (22.4 +/- 3.3 versus 29.9 +/- 5.9 mm/m2, P < 0.05) and a higher preoperative ejection fraction (53 +/- 8% versus 37 +/- 13%, P < 0.01). Dobutamine infusion augmented the difference in ventricular size and function between patients in group 1 and those in group 2 (LV end-systolic dimension index 18.9 +/- 3.9 mm/m2 versus 28.8 +/- 7.1 mm/m2, P < 0.01; ejection fraction 61 +/- 7% versus 41 +/- 12%, P < 0.01). CONCLUSIONS: Dobutamine accentuates differences in ventricular size and function between those with and without subsequent complete recovery following valve surgery. Because preoperative ejection fraction during LDDE is highly predictive of postoperative ejection fraction, LDDE may have a role in predicting the clinical outcome of patients following aortic valve replacement for aortic regurgitation.     

Left ventricular remodeling early after aortic valve replacement: differential effects on diastolic function in aortic valve stenosis and aortic regurgitation

OBJECTIVES: The aim of this study was to evaluate the effect of aortic valve replacement (AVR) on left ventricular (LV) function and LV remodeling, comparing patients with aortic valve stenosis to patients with aortic regurgitation. BACKGROUND: Aortic valve disease is associated with eccentric or concentric LV hypertrophy and changes in LV function. The relationship between LV geometry and LV function and the effect of LV remodeling after AVR on diastolic filling, in patients with aortic valve stenosis compared with aortic regurgitation, are largely unknown.Nineteen patients with aortic valve disease (12 aortic valve stenosis, 7 aortic regurgitation) were studied using magnetic resonance imaging to assess LV geometry and LV function before and 9 +/- 3 months after AVR. Ten age-matched healthy males served as control subjects. RESULTS: Before AVR, the ratio between left ventricular mass index (LVMI) and left ventricular end-diastolic volume index (LVEDVI) was only increased in patients with aortic valve stenosis (1.37 +/- 0.16 g/ml) compared with control subjects (0.93 +/- 0.08 g/ml, p < 0.05). After AVR, LVMI/LVEDVI decreased significantly in aortic valve stenosis (to 1.15 +/- 0.14 g/ml, p < 0.0001), but increased significantly in aortic regurgitation (1.02 +/- 0.20 g/ml to 1.44 +/- 0.27 g/ml, p < 0.0001). Before AVR, diastolic filling was impaired in both aortic valve stenosis and aortic regurgitation. Early after AVR, diastolic filling improved in patients with aortic valve stenosis, whereas patients with aortic regurgitation showed a deterioration in diastolic filling. CONCLUSIONS: Early after AVR, patients with aortic valve stenosis show a decrease in both LVMI and LVMI/LVEDVI and an improvement in diastolic filling, whereas in patients with aortic regurgitation, LVMI decreases less rapidly than LVEDVI, causing concentric remodeling of the LV, most likely explaining the observed deterioration of diastolic filling in these patients.     

Aortic valve stenosis: comparison of patients with to those without chronic congestive heart failure

Eighty-four patients with aortic valve stenosis (AS) and without other valvular or coronary artery disease were studied to investigate the pathophysiologic importance of hemodynamic and functional factors in the development of congestive heart failure (CHF). Thirty had clinical and radiographic signs of CHF. There was no significant difference between patients with and those without CHF in aortic valve index (0.26 +/- 0.09 vs 0.34 +/- 0.16 cm2/m2), mean aortic valve gradient (64 +/- 19 vs 59 +/- 25 mm Hg), left ventricular (LV) systolic pressure (201 +/- 31 vs 201 +/- 35 mm Hg), LV end-diastolic diameter (4.8 +/- 1.0 vs 4.4 +/- 0.7 cm) or posterior LV wall thickness (14.0 +/- 4.7 vs 15.0 +/- 30.0 mm). Patients with CHF had higher LV end-diastolic pressure (22 +/- 10 vs 16 +/- 7 mm Hg, p less than 0.005) and LV wall stress (370 +/- 138 vs 300 +/- 69 g/cm2, p less than 0.005) and lower cardiac index (2.0 +/- 0.5 vs 2.4 +/- 0.6 liters/min/m2, p less than 0.005) and LV ejection fraction (55 +/- 18 vs 68 +/- 13%, p less than 0.0005). An inverse linear relation (r = -0.59, p less than 0.01) was present between LV wall stress and LV ejection fraction such that as stress increased, LV ejection fraction fell. Values for both LV wall stress and LV ejection fraction overlapped considerably between the groups and, more important, only 40% of patients with CHF had a depressed LV ejection fraction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Course of the radionuclide left ventricular ejection fraction at rest and during exercise in surgically treated asymptomatic chronic aortic insufficiency

In order to preserve left ventricular (LV) function, aortic valve replacement may be contemplated in asymptomatic patients with aortic regurgitation when LV dilatation and dysfunction are not too advanced. Our study involved 10 asymptomatic patients with severe, isolated and pure aortic regurgitation. Before, and 6 months after the operation, the LV ejection fraction (LVEF) was measured at rest and during exercise on an ergometric bicycle by radionuclide angiography (multigated technique). Mean preoperative values were: age 52 +/- 14 years; cardiothoracic ratio 0.55 +/- 0.04; end-diastolic LV diameter 69 +/- 9 mm; end systolic LV diameter 47 +/- 7 mm; LV fibre shortening fraction 0.31 +/- 0.03; LVEF 0.55 +/- 0.10 at rest and 0.41 +/- 0.13 at exercise. After surgery, the cardiothoracic ratio value (0.51 +/- 0.03) and the LVEF value at rest (0.60 +/- 0.07) were not significantly different from the corresponding preoperative values, but the LVEF value during exercise was significantly increased (0.58 +/- 0.11, p less than 0.001). Among the 9 patients who before surgery showed a fall in LVEF at exercise, after surgery 5 had a rise (group B) and 4 had a fall (group A) in LVEF at exercise. Before surgery, group A patients had greater LV diameters than group B patients: end-diastolic diameter 76 +/- 6 mm vs 63 +/- 9 mm; end-systolic diameter 53 +/- 4 mm vs 43 +/- 7 mm (p = 0.07). These diameters were the only variables that predicted the postoperative changes in LVEF at exercise.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hemodynamic effects of nitroprusside on valvular aortic stenosis.

The effects of acute reduction of left ventricular (LV) loading in valvular aortic stenosis (AS) were examined. Thirty-five consecutive patients with AS (peak-to-peak aortic valve gradient 66 +/- 26 mm Hg, aortic valve area 0.65 +/- 0.22 cm2) were given intravenous sodium nitroprusside (1 to 3 micrograms/kg/min) to reduce systolic aortic pressures by greater than 10 mm Hg (mean aortic pressure 99 +/- 15 to 80 +/- 15 mm Hg; p less than 0.001). Overall, nitroprusside infusion resulted in little change in cardiac index (2.72 +/- 0.61 to 2.67 +/- 0.58 liters/min/m2; p = not significant). Individual patients had a range of responses. Fourteen patients (group 1) had an increase in cardiac index (2.42 +/- 0.59 to 2.74 +/- 0.67 liters/min/m2; p less than 0.001), whereas 21 (group 2) had a decrease or no change (2.93 +/- 0.56 to 2.61 +/- 0.52 liters/min/m2; p less than 0.001). Comparison of these subgroups showed that a cardiac index increase with nitroprusside was significantly predicted by a higher LV end-diastolic pressure (26 +/- 12 vs 15 +/- 6 mm Hg), lower LV ejection fraction (44 +/- 18 vs 62 +/- 12%). smaller aortic valve area (0.52 +/- 0.12 vs 0.74 +/- 0.22 cm2) and lower cardiac index (2.42 +/- 0.59 vs 2.93 +/- 0.56 liters/min/m2) (all values groups 1 and 2, respectively). It is concluded that there is a disparate response to acute vasodilatation in AS. Potentially beneficial effects are seen in a subgroup of patients, especially those with increased filling pressures and impaired LV function.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Ventricular arrhythmias in mitral valve disease: incidence, severity and relations to hemodynamic parameters

The incidence and severity of ventricular arrhythmias was analyzed in 42 patients with pure or predominant mitral valve stenosis (age: 51 +/- 9 years; NYHA class: 2.7 +/- 0.5) and 23 patients with pure or predominant mitral valve regurgitation (age: 55 +/- 11 years; NYHA class: 2.7 +/- 0.6) employing 24 h ambulatory monitoring. Coronary artery disease was excluded by angiography in all patients. Ten patients (14%) had no ventricular premature beats (VPB), 5 patients (7%) greater than 1,000 VPB/24 h, 31 patients (44%) multiform VPB, 19 patients (27%) repetitive VPB and 7 patients (10%) ventricular tachycardia. There was no difference in VPB between patients with mitral valve stenosis and mitral valve regurgitation. The incidence and severity of ventricular arrhythmias was significantly higher (p less than 0.001) in patients with mitral valve disease compared to the VPB of 50 normals without identifiable heart disease. This was still valid, if only patients with normal left ventricular ejection fraction greater than 55% (n = 60) were compared (p less than 0.01). The occurrence of frequent and complex ventricular arrhythmias was not determined by age, NYHA class, pulmonary artery pressure, pulmonary artery resistance, size of the left atrium, mitral valve area, degree of mitral regurgitation or cardiac index. However, a significant inverse correlation was found between incidence and severity of VPB and left ventricular ejection fraction. A reduced right ventricular ejection fraction, on the other hand, barely affected the occurrence of complex ventricular arrhythmias. Thus frequent and complex ventricular arrhythmias may be a sign of reduced left ventricular function in patients with mitral valve disease.     

Relationship of contractile state to ejection performance in patients with chronic aortic valve disease

To assess the relative contributions of afterload mismatch and impaired contractility to pump dysfunction in patients with chronic aortic valve disease, simultaneous left ventricular cineangiography and micromanometry were performed in 56 patients: 21 with severe aortic stenosis, 16 with severe aortic regurgitation, and 19 normal control subjects. Left ventricular mass was increased in patients with aortic stenosis and aortic regurgitation (172 +/- 52 and 224 +/- 63 g/m2, respectively, vs 89 +/- 16 for control subjects; p less than .05) as were end-diastolic volume (101 +/- 39 and 167 +/- 44 vs 77 +/- 16 ml/m2; p less than .05) and end-systolic volume (50 +/- 40 and 84 +/- 43 vs 24 +/- 7 ml/m2; p less than .05). Although ejection fraction was depressed in both abnormal groups (0.56 +/- 0.18 for patients with aortic stenosis and 0.53 +/- 0.13 for those with aortic regurgitation vs 0.69 +/- 0.05 for control subjects; p less than .05), the decrease in ejection fraction was disproportionate to the mild degree of afterload mismatch (end ejection stress 129 +/- 17 in patients with aortic stenosis and 154 +/- 58 in those with aortic regurgitation vs 117 +/- 46 kdyn/cm2 in control subjects; p = NS) with 10 of 21 patients with aortic stenosis and 12 of 16 patients with aortic regurgitation falling below the 95% prediction limit of the linear inverse relationship between ejection fraction and end-systolic stress for controls (EF = 0.78 - 0.00074 X ESS).(ABSTRACT TRUNCATED AT 250 WORDS)     

Importance of the "atrial kick" in determining the effective mitral valve orifice area in mitral stenosis

Atrial fibrillation with a rapid ventricular response in patients with mitral stenosis (MS) is often accompanied by pulmonary congestion and reduced cardiac output owing to a diminished diastolic filling period and the loss of the end-diastolic left ventricular (LV) pressure increment. To test the hypothesis that loss of atrial contraction (atrial kick) also results in a decrease in effective mitral valve orifice area, 6 patients with pure, isolated MS were studied in sinus rhythm during atrial pacing and simultaneous atrioventricular pacing. Atrial pacing at 140 beats/min caused no significant change from baseline in cardiac output or mitral valve area, but there was a decrease in LV end-diastolic volume and ejection fraction as well as an increase in left atrial pressure and mean diastolic gradient. Simultaneous atrioventricular pacing (to eliminate atrial kick) induced a decrease in cardiac output (4.4 +/- 0.9 vs 5.2 +/- 0.8 liters/min at 110 beats/min, 4.2 +/- 0.9 vs 5.1 +/- 0.9 liters/min at 140 beats/min; p less than 0.05) and LV end-diastolic volume (77 +/- 27 vs 93 +/- 29 ml at 110 beats/min, 54 +/- 17 vs 65 +/- 19 ml at 140 beats/min; p less than 0.05), an increase in left atrial pressure (28 +/- 3 vs 20 +/- 5 mm Hg at 110 beats/min, 30 +/- 4 vs 25 +/- 5 mm Hg at 140 beats/min; p less than 0.05), and a decrease in mitral valve area (1.2 +/- 0.4 vs 1.4 +/- 0.5 cm2 at 110 beats/min, 1.2 +/- 0.4 vs 1.4 +/- 0.4 cm2 at 140 beats/min; p less than 0.05). Thus, loss of atrial kick may cause pulmonary congestion and reduced cardiac output in patients with MS, partly because of a decrease in effective mitral valve area.     

Left ventricular remodeling after aortic valve replacement]

The aim of the study was the assessment of left ventricular (LV) systolic function and left ventricular mass following aortic valve replacement (AVR) due to aortic valve stenosis as well as the influence of regression of LV hypertrophy in patients with normal and impaired LV systolic function prior to surgery. 74 patients with severe aortic valve stenosis (29 female, 45 male, mean age 66 +/- 18 years) were divided into 2 groups according to LV ejection fraction (EF): Group 1 with EF > 50% (n = 40); Group 2 with EF < or = 50% (n = 34). Furthermore, patients were differentiated into a group A without (n = 53) and a group B with aortic regurgitation (< or = II degrees, n = 21). All patients were examined by transthoracic echocardiography before and 1 month after surgery. There was a significant decrease of LV enddiastolic and endsystolic volume indices following AVR in group 2 and group B. Patients with preoperatively lower EF (group 2) showed an increase in LV ejection fraction from 39 +/- 10% before AVR to 47 +/- 11% after AVR (p < 0.001), whereas patients with preoperative normal EF (group 1) showed a significant decrease in EF (from 62 +/- 8% to 57 +/- 10%, p < 0.05). Also patients with combined aortic valve disease before AVR had an increase of EF after surgery (from 45 +/- 14% to 56 +/- 14%, p < 0.03). There were significant decreases of interventricular septum thickness and LV posterior wall thickness in group 1 and group A, whereas a significant decrease of LV enddiastolic diameter index was noted only in group B. Improvement of the NYHA functional class could be demonstrated in group 2 from 2.8 +/- 0.7 before to 2.2 +/- 0.6 after AVR, as well as in group B from 2.9 +/- 0.7 before to 1.9 +/- 0.7 after surgery. In conclusion, patients with impaired LV function or combined aortic valve disease showed a significant improvement of left ventricular systolic function after AVR, while patients with normal LV function presented a slight decrease of EF. There was a significant regression of left ventricular muscle mass in all groups independent of the left ventricular functional status.     

Analysis of perioperative ventricular arrhythmias in valvular heart diseases by Holter ECG recording.

Seventy-one consecutive patients undergoing cardiac surgery for acquired valvular diseases were analyzed to determine the incidence of and the predisposing factors to postoperative ventricular arrhythmias. We recorded the Holter ECGs before (pre-op), and within 24h (op-day) and 4 to 10 weeks after operation (post-op) and determined the frequency of ventricular arrhythmias and the degree according to the Lown grade. The relationship between the op-day ventricular arrhythmias and clinical, hemodynamic, operative or postoperative variables was examined. The operation included mitral valve replacement or open mitral commissurotomy (49 patients, group M), aortic valve replacement (12 patients, group A) and a combined mitral and aortic operation (10 patients, group A + M). In all groups, the frequency and the degree of ventricular arrhythmias increased at the op-day and decreased at the post-op period approximately to the pre-op level. The frequency and Lown grade of the 3 groups were similar in each of the pre-op, the op-day and the post-op periods. The frequency and Lown grade of the op-day ventricular arrhythmias increased with increases in the arrhythmia frequency and Lown grade at the pre-op period, and in patients with left ventricular (LV) dysfunction at the post-op period, as evidence by an increased LV volume and decreased ejection fraction on echocardiograms. Furthermore, the frequency of ventricular premature contractions in the op-day was significantly less when a cardioplegia solution containing magnesium was used than in the case of a cardioplegia solution without magnesium. The op-day ventricular arrhythmias showed no significant relation to extracorporeal circulation time, aortic cross-clamping time, the antiarrhythmic drugs used and the op-day serum levels of K and CK-MB.     

Coronary flow reserve improves after aortic valve replacement for aortic stenosis: an adenosine transthoracic echocardiography study

OBJECTIVES: The goal of this study was to assess coronary flow reserve (CFR) before and after aortic valve replacement (AVR). BACKGROUND: Coronary flow reserve is impaired under conditions of left ventricular (LV) hypertrophy. It is not known whether CFR improves with regression of LV hypertrophy in humans. METHODS: We investigated 35 patients with pure aortic stenosis, LV hypertrophy and normal coronary arteriograms. Patients underwent adenosine transthoracic echocardiography on two occasions--immediately before AVR and six months postoperatively. Left ventricular mass, distal left anterior descending coronary artery (LAD) diameter, flow and CFR were assessed on each occasion. RESULTS: Distal LAD diameter was successfully imaged in 30 patients (86%), and blood flow was successfully imaged in 27 (77%). Paired data were subsequently available in 24 patients, of whom 14 were men, mean age 68.1+/-12.5 years, body mass index 24.5+/-2.0 kg/m2, aortic valve gradient 93+/-32 mm Hg. Pre- to post-AVR a significant decrease was seen in LV mass (271+/-38 vs. 236+/-32g, p<0.01) and LV mass index (154+/-21 vs. 134+/-21 g/m2, p< 0.01). Distal LAD diameter fell from 2.27+/-0.37 to 2.23+/-0.35 mm, p = 0.08). Pre- to post-AVR there was no significant change in resting parameters of peak diastolic velocity (0.43+/-0.16 vs. 0.41+/-0.11 m/s), distal LAD flow 23.3+/-10.1 vs. 20.9+/-5.2 ml/min or distal LAD flow scaled for LV mass (8.7+/-3.8 vs. 9.0+/-2.5 ml/min/100 g LV mass), but there was significant increase in hyperemic peak diastolic velocity (0.71+/-0.26 vs. 1.08+/-0.24 m/s; p<0.01), distal LAD flow (37.8+/-11.3 vs. 53.5+/-16.1 ml/min; p<0.01) and distal LAD flow scaled for LV mass (14.3+/-5.0 vs. 23.3+/-8.5 ml/min/100 g LV mass; p<0.01). Coronary flow reserve, therefore, increased from 1.76+/-0.5 to 2.61+/-0.7. CONCLUSIONS: Coronary flow reserve increases after AVR for aortic stenosis. This increase occurs in tandem with regression of LV hypertrophy.     

Influence of left ventricular mass on coronary artery cross-sectional area

Observations from cardiac catheterization suggest that coronary artery cross-sectional area (CSA) is increased in patients with left ventricular (LV) hypertrophy and is proportional to LV mass. This hypothesis was tested using computer-based quantitative analysis of LV mass and CSA from angiographic images of the left ventricle and proximal coronary arteries from 19 men and 21 women, aged 23 to 78 years (mean 56). Twenty-seven patients had valvular heart disease, 16 of whom had multivalvular involvement; diagnoses included aortic stenosis in 19, aortic regurgitation in 13 and mitral regurgitation in 12. Thirteen patients had normal valvular and ventricular function. All patients had normal coronary arteries. Significant differences between normal patients and those with valvular disease were noted in LV mass (88 +/- 7 vs 165 +/- 12 g/m2, p less than 0.001) and coronary CSA (26 +/- 2 vs 46 +/- 3 mm2, p less than 0.001). Furthermore, a linear relation between LV mass and coronary CSA was noted (r = 0.788, p less than 0.001). Thus, proximal coronary artery CSA is significantly larger in valvular heart disease patients with LV hypertrophy than in those with normal ventricles, and proximal coronary artery area increases in proportion to LV mass in hypertrophied ventricles.     

Effects of valve replacement on left ventricular function in patients with aortic regurgitation and severe ventricular disease

BACKGROUND AND AIM OF THE STUDY: Longstanding aortic regurgitation (AR) can result in left ventricular (LV) dysfunction that may reverse after aortic valve replacement (AVR). Stentless valves may result in a more rapid recovery in function due to a more physiological flow and lower outflow resistance. METHODS: The effect of AVR on LV function was studied in 47 patients who received either a stentless (n = 33) or stented (n = 14) valve for isolated AR. All patients had evidence of pre-existing LV dysfunction (end-systolic dimension (ESD) >50 mm). Patients were studied using transthoracic echocardiography at baseline, postoperatively, and at 2.5-year follow up. RESULTS: Preoperatively, there were no differences in LV dimensions. The end-diastolic dimension fell from 75 +/- 10 mm to 61 +/- 10 mm postoperatively and to 52 +/- 10 mm at follow up in the stentless group (p <0.001), and ESD fell from 54 +/- 10 mm to 36 +/- 8 mm at follow up (p <0.001). There were no significant early changes in patients who received stented valves, though LV dimensions fell at follow up. Fractional shortening (FS) increased from 25 +/- 8% in the postoperative period to 31 +/- 7% in the stentless group (p <0.001), but there was no change in the stented group (20 +/- 7% versus 23 +/- 8%). In the stentless group, LV mass fell from 366 +/- 104 g to 276 +/- 68 g postoperatively and to 219 +/- 79 g at follow up (p <0.001); there was no postoperative change in the stented group, though a late reduction occurred, from 349 +/- 51 g preoperatively to 265 +/- 61 g at follow up (p = 0.06). CONCLUSION: For patients with AR and LV dysfunction, AVR with a stentless prosthesis offers early reductions in LV dimensions, improved LV function, and regression of LV mass. In patients who received a stented valve, these improvements were delayed and less complete. Hence, for some patients with AR and LV dysfunction, a stentless prosthesis may be preferable.     

Effect of volume load of the left ventricle in aortic and mitral insufficiency on the geometry and function of the right ventricle

To investigate the effect of chronic left ventricular enlargement on right ventricular geometry and function, biplane cineventriculograms were analyzed in 23 patients with aortic regurgitation (AR) and in 17 patients with mitral regurgitation (MR). Left ventricular end-diastolic volume indices (LVEDVI) were elevated and significantly (p less than 0.05) different in patients with aortic regurgitation (AR) (190.2 +/- 65.2 ml/m2) and mitral regurgitation (MR) (148.7 +/- 40.1 ml/m2). Right ventricular end-diastolic volume indices (RVEDVI), however, were comparable and within the normal range (AR: 96.6 +/- 18.3 ml/m2, MR: 100.2 +/- 33.7 ml/m2). Mean pulmonary artery pressure was significantly (p less than 0.05) higher in patients with mitral regurgitation with 24.7 +/- 12.8 mm Hg (AR: 17.5 +/- 6.6 mm Hg). Six patients with mitral insufficiency had concomitant tricuspid valve insufficiency. In five out of six patients with tricuspid insufficiency, right ventricular afterload was significantly elevated. Only in patients with mitral regurgitation was a significant correlation (r) between left and right ventricular end-diastolic volume index found (RVEDVI = 0.7 X LVEDVI +1, r = 0.80). Moreover, in patients with MR, left ventricular end-diastolic volume index correlated with right ventricular end-systolic volume index (RVESVI = 0.4 X LVEDVI -8, r = 0.73). Right ventricular ejection fraction was significantly different (p less than 0.05) between patients with aortic and mitral insufficiency (AR: 53.7 +/- 8.9%, MR: 46.7 +/- 10.7%). Particularly in patients with normal left ventricular ejection fraction (greater than 50%) and mitral regurgitation, the incidence of a reduced right ventricular ejection fraction (less than 50%) was significantly higher (p less than 0.01) compared to patients with aortic regurgitation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Early autonomic and repolarization abnormalities contribute to lethal arrhythmias in chronic ischemic heart failure: characteristics of a novel heart failure model in dogs with postmyocardial infarction left ventricular dysfunction

OBJECTIVES: Using a model of arrhythmias associated with ischemic left ventricular (LV) dysfunction, this study investigated autonomic and electrophysiologic mechanisms associated with sudden cardiac death (SCD) in chronic heart failure (HF). BACKGROUND: Left ventricular dysfunction from ischemic heart disease is associated with many instances of SCD. Electrophysiologic and autonomic derangements occur in HF, but their contribution to SCD risk is poorly understood. METHODS: Sudden death risk was assessed in 15 dogs with a healed anterior myocardial infarction (MI) during submaximal exercise and brief acute circumflex ischemia. Left ventricular dysfunction was then induced by repetitive circumflex microembolization until LV ejection fraction reached 35%. Before embolization, six dogs were susceptible to SCD, and nine were resistant. RESULTS: Baroreflex sensitivity was lower in susceptible dogs (10 ms/mm Hg +/- 4 ms/mm Hg vs. 20 ms/mm Hg +/- 11 ms/mm Hg, p = 0.04). QT intervals from susceptible dogs were longer after MI (246 ms +/- 26 ms susceptible vs. 231 ms +/- 20 ms resistant, p < 0.001) and prolonged within eight weeks after LV dysfunction was established (from 246 ms +/- 26 ms to 274 ms +/- 56 ms, +11%, p < 0.01). Heart rate in susceptible dogs increased during transient ischemia (+20%) and with progressive LV dysfunction (102 beats/min +/- 28 beats/min baseline to 154 beats/min +/- 7 beats/min LV dysfunction, p = 0.003). All susceptible dogs had spontaneous sustained ventricular tachycardia culminating in SCD. In contrast, QT intervals in resistant dogs prolonged after 24 +/- 6 weeks (from 231 ms +/- 20 ms to 238 ms +/- 15 ms, p < 0.05), and heart rates were unchanged. Only one resistant dog died suddenly with LV dysfunction. CONCLUSIONS: Depressed vagal and elevated sympathetic control of heart rate coupled with abnormal repolarization are associated with high SCD risk when post-MI LV dysfunction develops.     

Radiofrequency catheter ablation of premature ventricular complexes from right ventricular outflow tract improves left ventricular dilation and clinical status in patients without structural heart disease

OBJECTIVES: The present study evaluated clinical benefits of radiofrequency catheter ablation (RFA) for premature ventricular complexes from right ventricular outflow tract (RVOT-PVC) in patients without structural heart disease. BACKGROUND: It is unknown whether PVC causes left ventricular (LV) dilation, which is a well-recognized precursor of LV dysfunction and heart failure, and whether eliminating PVC by RFA produces clinical benefits in patients with RVOT-PVC. METHODS: Frequency of PVC per total heart beats by 24-h Holter monitoring, left ventricular ejection fraction (LVEF), left ventricular end-diastolic internal dimension (LVDd), mitral regurgitation (MR) by echocardiogram, cardiothoracic ratio (CTR) by chest radiogram, and New York Heart Association (NYHA) functional class of 40 patients with RVOT-PVC without structural heart disease were evaluated before and 6 to 12 months after RFA. RESULTS: Before RFA, a subgroup of patients with frequent (>20%) PVC demonstrated significantly enlarged LVDd and CTR, reduced LVEF, increased MR, and deteriorated NYHA functional class as compared to the subgroup with rare (<20%) PVC (54 +/- 1 mm vs. 45 +/- 1 mm, 52 +/- 2% vs. 46 +/- 1%, 66 +/- 2% vs. 73 +/- 2%, 1.2 +/- 0.2 degree vs. 0.4 +/- 0.1 degree, and 1.8 +/- 0.2 vs. 1.3 +/- 0.1, respectively; p < 0.05). Furthermore, ablating RVOT-PVC readily produced the improvement of all these abnormalities (47 +/- 1 mm, 41 +/- 1%, 72 +/- 2%, 0.3 +/- 0.1 degree, and 1.0 +/- 0.0, respectively; p < 0.05 compared with before RFA). CONCLUSIONS: These findings suggest that frequent (>20%) RVOT-PVC may be a possible cause of LV dysfunction and/or heart failure, and RFA produces clinical benefits in these patients.