Echocardiography in the critically ill: current and potential roles.

BACKGROUND: The use of echocardiography in the critically ill presents specific challenges. However, information of direct relevance to clinical management can be obtained relating to abnormalities of structure and function and can be used to estimate pulmonary arterial and venous pressures. DISCUSSION: Investigation of the consequences of myocardial ischaemia, valvular dysfunction and pericardial disease can be facilitated, and changes characteristic of specific conditions (e.g. sepsis, pulmonary thromboembolism) detected. Echocardiography can also be used to monitor the effects of therapeutic interventions. CONCLUSIONS: The applications of echocardiography in the critical care setting (excluding standard peri-operative echocardiography for cardiac surgery) are reviewed, with particular emphasis on the assessment of cardiac physiology.

Stress-induced left ventricular outflow tract obstruction: a potential cause of dyspnea in the elderly.

OBJECTIVES: We sought to identify the pattern of disturbed left ventricular physiology associated with symptom development in elderly patients with effort-induced breathlessness. BACKGROUND: Limitation of exercise tolerance by dyspnea is common in the elderly and has been ascribed to diastolic dysfunction when left ventricular cavity size and systolic function appear normal. METHODS: Dobutamine stress echocardiography was used in 30 patients (mean [+/-SD] age 70 +/- 12 years; 21 women, 9 men) with exertional dyspnea and negative exercise test results, and the values were compared with those in 15 control subjects. RESULTS: Before stress, left ventricular end-diastolic and end-systolic dimensions were reduced, fractional shortening was increased, and the basal septum was thickened (2.3 +/- 0.5 vs. 1.4 +/- 0.2 cm, p < 0.001, vs. control subjects) in the patients, but posterior wall thickness did not differ from that in control subjects. Left ventricular outflow tract diameter, measured as systolic mitral leaflet septal distance, was significantly reduced (13 +/- 4.5 vs. 18 +/- 2 mm, p < 0.001). Isovolumetric relaxation time was prolonged, and peak left ventricular minor axis lengthening rate was reduced (8.1 +/- 3.5 vs. 10.4 +/- 2.6 cm/s, p < 0.05), suggesting diastolic dysfunction. Transmitral velocities and the E/A ratio did not differ significantly. At peak stress, heart rate increased from 66 +/- 8 to 115 +/- 20 beats/min in the control subjects, but blood pressure did not change. Transmitral A wave velocity increased, but the E/A ratio did not change. Left ventricular outflow tract velocity increased from 0.8 +/- 0.1 to 2.0 +/- 0.2 m/s, and mitral leaflet septal distance decreased from 18 +/- 2 to 14 +/- 3 mm, p < 0.001. In the patients, heart rate rose from 80 +/- 12 to 132 +/- 26 beats/min and systolic blood pressure from 143 +/- 22 to 170 +/- 14 mm Hg (p < 0.001 for each), but left ventricular dimensions did not change. Peak left ventricular outflow tract velocity increased from 1.5 +/- 0.5 m/s (at rest) to 4.2 +/- 1.2 m/s; mitral leaflet septal distance fell from 13 +/- 4.5 to 2.2 +/- 1.9 mm (p < 0.001); and systolic anterior motion of mitral valve appeared in 24 patients (80%) but in none of the control subjects (p < 0.001). Measurements of diastolic function did not change. All patients developed dyspnea at peak stress, but none developed a new wall motion abnormality or mitral regurgitation. CONCLUSIONS: Although our patients fulfilled the criteria for "diastolic heart failure," diastolic dysfunction was not aggravated by pharmacologic stress. Instead, high velocities appeared in the left ventricular outflow tract and were associated with basal septal hypertrophy and systolic anterior motion of the mitral valve. Their appearance correlated closely with the development of symptoms, suggesting a potential causative link.

Angiotensin-converting enzyme (ACE) inhibitors revert abnormal right ventricular filling in patients with restrictive left ventricular disease.

OBJECTIVES: Our aim was to determine mechanisms underlying abnormalities of right ventricular (RV) diastolic function seen in heart failure. BACKGROUND: It is not clear whether these right-sided abnormalities are due to primary RV disease or are secondary to restrictive physiology on the left side of the heart. The latter regresses with angiotensin-converting enzyme inhibition (ACE-I). METHODS: Transthoracic echo-Doppler measurements of left- and right-ventricular function in 17 patients with systolic left ventricular (LV) disease and restrictive filling before and 3 weeks after the institution of ACE-I were compared with those in 21 controls. RESULTS: Before ACE-I, LV filling was restrictive, with isovolumic relaxation time short and transmitral E wave acceleration and deceleration rates increased (p < 0.001). Right ventricular long axis amplitude and rates of change were all reduced (p < 0.001), the onset of transtricuspid Doppler was delayed by 160 ms after the pulmonary second sound versus 40 ms in normals (p < 0.001) and overall RV filling time reduced to 59% of total diastole. Right ventricular relaxation was very incoordinate and peak E wave velocity was reduced. Peak RV to right atrial (RA) pressure drop, estimated from tricuspid regurgitation, was 45+/-6 mm Hg, and peak pulmonary stroke distance was 40% lower than normal (p < 0.001). With ACE-I, LV isovolumic relaxation time lengthened, E wave acceleration and deceleration rates decreased and RV to RA pressure drop fell to 30+/-5 mm Hg (p < 0.001) versus pre-ACE-I. Right ventricular long axis dynamics did not change, but tricuspid flow started 85 ms earlier to occupy 85% of total diastole; E wave amplitude increased but acceleration and deceleration rates were unaltered. Values of long axis systolic and diastolic measurements did not change. Peak pulmonary artery velocity increased (p < 0.01). CONCLUSIONS: Abnormalities of RV filling in patients with heart failure normalize with ACE-I as restrictive filling regresses on the left. This was not due to altered right ventricular relaxation or to a fall in pulmonary artery pressure or tricuspid pressure gradient, but appears to reflect direct ventricular interaction during early diastole.

Electromechanical left ventricular behavior after nonsurgical septal reduction in patients with hypertrophic obstructive cardiomyopathy.

OBJECTIVES: To investigate the electromechanical consequences of nonsurgical septal reduction in a group of patients with hypertrophic obstructive cardiomyopathy (HOCM). BACKGROUND: Patients with HOCM may benefit symptomatically from nonsurgical septal reduction as an alternative to dual chamber pacing and sensing (DDD) pacing and surgical myectomy. METHODS: We studied 20 symptomatic patients with HOCM (12 men), mean age 52 +/- 17 years, before and after septal reduction using echocardiography and electrocardiogram (ECG). RESULTS: Septal reduction with a significant rise in cardiac enzymes was successfully achieved in all patients resulting in a 50% reduction in resting left ventricular (LV) outflow tract gradient within 24 h of procedure and an 80% reduction after six months. Left ventricular outflow tract diameter increased at 24 h with a further increase six months later. QRS duration increased by 35 ms at 24 h after procedure associated with right bundle branch block (RBBB) and significant rightward axis rotation in 16 patients. R-wave amplitude in V1 fell by 7 +/- 4 mm in 15/20 patients, 13 of whom developed reduction of septal long axis excursion. Left-axis deviation appeared in three patients and septal q-wave was suppressed in 12 long-axis excursion; peak shortening and lengthening rates all fell at the septal site by 20% at 24 h. Only septal excursion returned back to baseline values at six months. Wall motion also became incoordinate so that postejection septal shortening increased by three times control values at 24 h and by four times six months later. CONCLUSIONS: Nonsurgical septal reduction is associated with a drop in LV outflow tract obstruction and the creation of a localized myocardial infarction (MI) increasing LV outflow tract diameter. The technique also results in a consistent alteration of septal activation and secondary incoordination. The latter could play a significant role in gradient reduction and symptomatic improvement in a manner similar to that seen with DDD pacing.

Effects of intravenous milrinone on left ventricular function in ischemic and idiopathic dilated cardiomyopathy.

M-mode echocardiography and Doppler were used to assess the effects of phosphodiesterase inhibition on subendocardial function in dilated cardiomyopathy, and in particular, to study interactions with both systolic and diastolic left ventricular function. Twelve adult patients with dilated cardiomyopathy were studied (6 ischemic in origin and 6 idiopathic), 7 of whom were being considered for cardiac transplantation. Cardiac index increased without significant change in heart rate or blood pressure. Longitudinal mitral ring motion, which had been uniformly reduced, increased markedly after intravenous milrinone. Left ventricular cavity size decreased, and shortening fraction, posterior wall thickness, and rates of posterior wall thickening and thinning increased markedly. Left atrial pressure decreased, and isovolumic relaxation time increased. However, the peak velocity and duration of the transmitral E wave increased, with no change in the A wave. Improved longitudinal (subendocardial) function was reflected by improved posterior wall dynamics, and early filling, possibly by augmentation of restoring forces. Thus, severely reduced subendocardial function in dilated cardiomyopathy is potentially reversible, with marked effects on systolic and diastolic function. These previously unrecognized actions of milrinone provide further evidence to justify its short-term use in supporting the severely depressed myocardium.

Comparison of intravenous nicardipine and nitroglycerin to control systemic hypertension after coronary artery bypass grafting.

The efficacy of intravenous (i.v.) nicardipine hydrochloride (a calcium antagonist) compared with nitroglycerin, the drug generally used for treatment of hypertension after coronary artery bypass grafting, was tested in 20 postoperative patients. The patients were randomly divided in a nonblinded manner into 2 groups. Baseline characteristics were similar in the 2 groups. Patients in both groups received various oral calcium antagonists. In addition, 1 group was treated with i.v. nitroglycerin. Both drugs were infused at a maximal rate of 30 mg/hour, as needed to maintain systolic blood pressure below 110 mm Hg. If blood pressure increased to more than 120 mm Hg, nitroprusside was administered. Intravenous nicardipine was superior to nitroglycerin in control of hypertension after coronary artery bypass grafting. In patients treated with nicardipine, blood pressure was decreased sooner (mean infusion time 7.7 hours vs 11.9 hours for nitroglycerin), mean systolic blood pressure was reduced (94 vs 108 mm Hg for the nitroglycerin group; p less than 0.05), and no patient required nitroprusside treatment (compared with 3 patients who required this treatment in the nitroglycerin group). There were no differences in heart rate, diastolic pressure, cardiac index and urine flow between the 2 treatment groups. No adverse effects were observed in patients treated with nicardipine.

Exercise echocardiography in children with Kawasaki disease: ventricular long axis is selectively abnormal.

In asymptomatic children with Kawasaki disease, left ventricular traditional markers of systolic and diastolic function are maintained. However, long-axis function, which represents the subendocardium, is abnormal during stress, particularly in patients with versus without coronary aneurysm.

Early changes in left ventricular function after aortic valve replacement for isolated aortic stenosis.

To assess the immediate effects of aortic valve replacement (AVR) for valvular aortic stenosis (AS) on left ventricular (LV) systolic and diastolic function and global hemodynamics, 17 patients with AS underwent transesophageal echocardiography combined with high-fidelity LV pressure recording and thermodilution cardiac output measurements before cardiopulmonary bypass and 0.5, 6, 12, and 20 hours after AVR. Compared with results before bypass, LV systolic function had already changed 30 minutes after AVR, and remained constant thereafter: peak LV systolic wall stress decreased (from 210 +/- 60 to 130 +/- 40 g.cm-2), peak rate of dimension shortening increased (from 7.3 +/- 2.2 to 9.7 +/- 2.1 cm.s-1), both p < 0.01. Peak segmental external power thus remained constant (16.6 +/- 6.7 vs 17.7 +/- 7.6 mW.cm-3); p = NS. Changes in LV diastolic function and global hemodynamics were delayed. The peak rate of ventricular pressure decrease, normalized to developed end-systolic pressure, increased (from 15 +/- 3.2 to 19 +/- 5.2 s-1) by 6 hours. The minimal ventricular pressure of early diastole decreased (from 8.9 +/- 4.9 to 4.3 +/- 3.7 mm Hg), the peak rate of dimension lengthening of early diastole increased (from 6.0 +/- 3.0 to 8.8 +/- 2.0 cm.s-1), and LV stroke volume index increased (from 24 +/- 7 to 31 +/- 6 ml.m-2) by 12 hours, all p < 0.01. LV incoordination, defined as the dimension changes during isovolumic periods, had also improved significantly at 20 hours. Heart rate and LV enddiastolic dimension did not change.(ABSTRACT TRUNCATED AT 250 WORDS)

Echocardiographic determinants of mortality in patients >67 years of age with chronic heart failure.

This study sought to assess the prognostic significance of echocardiographic measurements of left and right ventricular dimensions and function in patients >67 years of age with chronic congestive heart failure (CHF). This is a retrospective follow-up of elderly patients who underwent an echocardiography in the tertiary cardiac center. A total of 185 patients (131 men) aged >/=68 years (mean +/- SD 75 +/- 5) with CHF were enrolled into the study. After undergoing a detailed echocardiographic examination, all patients were followed-up for a median of 20 months (interquartile range 9 to 36). During the follow-up period 54 patients (29%) died. Left ventricular (LV) M-mode isovolumic relaxation time (IVRT), end-diastolic and end-systolic diameters, fractional shortening and mass, transmitral E:A ratio, and left atrial dimension, as well as New York Heart Association class and the age were found by Cox proportional-hazards univariate analyses to predict the outcome in these patients (all p <0.05). In multivariate analyses including these measurements, LV IVRT (p <0.04), age (p <0.03), and New York Heart Association class (p <0.001) were found to be the independent predictors of outcome. In the Kaplan-Meier analysis, patients with LV IVRT >30 ms had a better prognosis at 3 years (cumulative survival 78% [95% confidence interval 65% to 91%]) than those with LV IVRT 67 years of age with CHF. LV M-mode IVRT is among the most important independent predictors of outcome in this population.

Abnormal ventricular long-axis function in systemic sclerosis.

STUDY OBJECTIVE: To assess possible effects of systemic sclerosis on ventricular function. DESIGN: Retrospective analysis of patients referred for echocardiographic examination to assess ventricular function. SETTING: Tertiary referral center for cardiac and chest diseases equipped with invasive and noninvasive facilities. PATIENTS: Thirty-four patients with clinical diagnosis of systemic sclerosis, aged 49 +/- 12 years; 24 had pulmonary fibrosis and 10 did not. There were 21 normal controls of similar age. MEASUREMENTS: Two-dimensional guided M-mode echocardiographic recordings of the left ventricular minor and long axis at the left and septal sites and right ventricle were obtained. Transmitral and transtricuspid Doppler flow velocities were also obtained with ECG and phonocardiogram. RESULTS: In 24 patients with pulmonary fibrosis, long-axis excursion was reduced 2.1 +/- 0.5 vs 2.7 +/- 0.4 cm/s as was peak rate of shortening and lengthening, 8.5 +/- 3.3 vs 10.8 +/- 2.4 cm/s and 7.5 +/- 2.5 vs 12 +/- 3.6 cm/s, respectively (p < 0.001), at the right side compared with 10 patients without. The onset of right long-axis shortening and lengthening was delayed with respect to the Q wave of the ECG and P2 of the phonocardiogram (p < 0.001 in both vs controls). The onset of tricuspid forward flow from the second heart sound was also delayed in the two groups, 110 +/- 15 ms and 100 +/- 20 ms vs 80 +/- 15 ms, respectively (p < 0.001). Right ventricular late diastolic filling velocities were increased 35 +/- 15 and 35 +/- 12 cm/s vs 20 +/- 10 cm/s in both groups (p < 0.01), and hence E:A ratio reduced 1.25 +/- 0.5 and 1.4 +/- 0.3 vs 1.9 +/- 0.4, respectively (p < 0.001). Pulmonary flow acceleration time was reduced only in patients with pulmonary fibrosis, 105 +/- 30 ms vs 125 +/- 30 ms (p < 0.001). At the left side, total long-axis excursion was reduced only in patients with pulmonary fibrosis (p < 0.01), while peak shortening and lengthening rates were reduced in both groups (p < 0.05). The onset of shortening from the Q wave and lengthening from the second heart sound were both delayed in the two groups with the latter greatly delayed in patients with pulmonary fibrosis (p < 0.05). CONCLUSIONS: Right and left ventricular long-axis function is frequently abnormal in patients with systemic sclerosis. Abnormalities are more profound in patients with CT evidence of pulmonary fibrosis than in those without. We suggest that these disturbances are due to myocardial fibrosis which, from the anatomic distribution of longitudinally directed fibers, is likely to have been subendocardial.

Right ventricular dysfunction in adult severe cystic fibrosis.

STUDY OBJECTIVES: This study sought to assess the extent of impairment of cardiac function in adult patients with end-stage cystic fibrosis (CF) and to examine the relationship between cardiovascular abnormalities and the degree of hypoxemia and hypercapnia. DESIGN AND SETTING: A retrospective study in a tertiary cardiac and CF center. PARTICIPANTS AND INTERVENTIONS: A total of 103 adult patients with end-stage CF awaiting lung or heart and lung transplantation (mean age [+/- SD], 26+/-7 years; 54 men) underwent Doppler echocardiography and arterial blood gas analysis (mean PaO(2), 54+/-10 mm Hg; mean PaCO(2), 47+/-8 mm Hg). The findings were compared to those of 17 healthy control subjects (mean age, 24+/-7 years; 13 men) who had no history of cardiac or pulmonary disease. MEASUREMENTS AND RESULTS: All patients were in sinus rhythm with a mean tachycardia of 112+/-18 beats/min (control subjects, 76+/-16; p<0.0001) and had a cardiac output of 5.3 L/min (control subjects, 4.3 L/min; p<0.04). In the patient group, the left ventricular (LV) dimensions, systolic and diastolic function, and wall thickness were all within normal limits. The mean amplitude of long-axis excursion in patients was normal at the LV site, but that of the right ventricular (RV) free wall was significantly reduced as compared with control subjects (1.6+/-0.4 vs. 2.2+/-0.4 cm, respectively; p<0.001), which was found to correlate with the degree of hypoxemia (r = 0.63; p<0.02) and hypercapnia (r = -0.68; p<0.01). RV diastolic function, which was represented by the relative isovolumic relaxation time to cardiac cycle length, was longer in patients than in control subjects (8.7+/-4.8% vs. 5.0+/-3.0%, respectively; p<0.03). The pulmonary flow acceleration time (90+/-22 vs 121+/-34 ms, respectively; p<0.01) and the systolic stroke distance (7.0+/-2.2 vs. 10.5+/-1.9 cm/s(2); p<0.001) were both lower than normal. CONCLUSIONS: This study confirms the presence of significant RV systolic and diastolic dysfunction in the setting of consistent tachycardia and increased cardiac output in adult CF patients with severe disease. No specific LV abnormalities were detected in these patients.

Management of tuberculous constrictive pericarditis and tuberculous pericardial effusion in Transkei: results at 10 years follow-up.

BACKGROUND: Tuberculous pericarditis is common in Transkei (Eastern Cape). Two randomized trials showed benefits at two years for prednisolone in patients with constrictive pericarditis, and open drainage plus prednisolone in patients with pericardial effusion. AIM: To see whether the advantages of prednisolone and open drainage were maintained up to 10 years. DESIGN: Follow-up of randomized, double-blind, placebo-controlled trials. METHODS: All 383 patients (143 constriction, 240 effusion) received the same anti-tuberculosis chemotherapy. They were randomized to prednisolone or placebo for the first 11 weeks, and were followed-up over 10 years. Among the 240 with effusion, 122 were also randomized to immediate open surgical drainage of pericardial fluid versus pericardiocentesis as required. Adverse outcomes were: death from pericarditis, pericardiectomy, repeat pericardiocentesis, and subsequent open drainage. RESULTS: The 10-year follow-up rate was 96%. In constriction patients, adverse outcomes occurred in 19/70 (27%) prednisolone vs. 28/73 (38%) placebo (p = 0.15), deaths from pericarditis being 2 (3%) vs. 8 (11%), respectively (p = 0.098, Fisher's exact test). In effusion patients, adverse outcomes occurred in 14/27 (52%) with neither drainage nor prednisolone, vs. 4/29 (14%) drainage and prednisolone, 4/35 (11%) drainage and placebo, and 6/31 (19%) prednisolone and no drainage (p = 0.08 for interaction). Drainage eliminated the need for repeat pericardiocentesis. In the 176 with effusion and no drainage, adverse outcomes occurred in 17/88 (19%) prednisolone vs. 35/88 (40%) placebo patients (p = 0.003), with repeat pericardiocentesis 20 (23%) placebo vs. 9 (10%) prednisolone (p = 0.025). In a multivariate survival analysis (stratified by type of pericarditis), prednisolone reduced the overall death rate after adjusting for age and sex (p = 0.044), and substantially reduced the risk of death from pericarditis (p = 0.004). At 10 years, the great majority of surviving patients in all treatment groups were either fully active or out and about, even if activity was restricted. DISCUSSION: In the absence of a clear contraindication, a corticosteroid should be used in addition to antituberculosis chemotherapy in the management of patients with tuberculous pericarditis.

The relationship of myocardial stroke work to coronary flow velocity immediately after aortic valve replacement.

BACKGROUND: The interrelations between myocardial stroke work and coronary flow velocity have not been fully defined during aortic valve replacement or with different cardioplegias. METHODS: Twenty-six patients (15 men age 63+/-13 years) who had elective isolated aortic valve replacement were studied by transesophageal Doppler echocardiography with simultaneous high fidelity left ventricular pressure. Fifteen patients received cold blood cardioplegia and 11 had warm blood cardioplegia. Myocardial stroke work and flow velocities in proximal left anterior descending coronary artery were quantified simultaneously before cardiopulmonary bypass and at 1, 6, 12, and 20 hours afterwards. RESULTS: Myocardial stroke work decreased postoperatively in both groups (160+/-19 versus 228+/-19 mJ/cm3 per minute, with cold blood cardioplegia; 135+/-22 versus 227+/-22 mJ/cm3 per minute with warm blood cardioplegia; both p<0.001 versus time, but p>0.05 versus cardioplegia, by two-way analysis of variance). Left anterior descending artery flow velocity-time integral per minute increased significantly in both groups (26.1+/-2.1 versus 15.0+/-2.1 m/min with cold blood cardioplegia; 32.8+/-2.5 versus 14.4+/-2.5 m/min with warm blood cardioplegia; both p<0.001 versus time, but p>0.05 versus cardioplegia). Thus, at 1 hour postoperatively the mJ x cm(-3) x m(-1) x min ratio of myocardial stroke work to left anterior descending artery flow velocity-time integral decreased significantly in both groups (4.3+/-1.6 versus 16.3+/-1.7 mJ x cm(-3) x m(-1) x min with warm blood cardioplegia, and 7.4+/-1.4 versus 17.9+/-1.4 J x cm(-3) x m(-1) x min with cold blood cardioplegia; both p<0.001 versus time). Warm blood cardioplegia was also associated with a lower mean ratio perioperatively than that with cold blood cardioplegia (7.8+/-0.9 versus 10.9+/-0.7 mJ x cm(-3) x m(-1) x min, p = 0.014). CONCLUSIONS: Coronary hyperemia occurs for at least 20 hours postoperatively when myocardial stoke work has decreased. The ratio of myocardial stroke work to coronary flow velocity appears to be more sensitive than either alone in differentiating the effect of warm versus cold blood cardioplegia.

Coronary artery problems during homograft aortic valve replacement: role of transesophageal echocardiography.

We describe 2 cases in which intraoperative transesophageal echocardiography detected complications related to the proximal coronary arteries during homograft aortic valve and root replacement. In both cases, cardiopulmonary bypass could not be discontinued despite the use of large doses of inotropic drugs. Transesophageal echocardiography demonstrated aliasing on color flow mapping in the left main coronary artery in 1 case and proximal right coronary artery in the other, along with severely depressed left ventricular anterior wall and right ventricular function, respectively. Coronary artery bypass grafting was performed in both cases, and the outcome was successful.

Perioperative assessment of aortic homograft, Toronto stentless valve, and stented valve in the aortic position.

We investigated aortic valve hemodynamic performance and perioperative left ventricular function in 50 patients (mean [+/- SD] age, 64 +/- 9 years; 34 men, 16 women) undergoing elective aortic valve replacement, using an aortic homograft (n = 20), a Toronto stentless porcine valve (n = 20), or a stented bioprosthesis (n = 10), by transesophageal echocardiography combined with high-fidelity cavity pressure recordings and thermodilution cardiac output measurements. Thirty-nine patients had aortic stenosis; 11 had predominant regurgitation. Thirteen patients with concomitant coronary artery stenosis underwent grafting. Left ventricular mass index in all patients was 280 +/- 110 g/m2. The transvalvular pressure drop and energy consumption were significantly higher with stented than stentless valves (5 with aortic homograft and 11 with Toronto valve, with matched age and valve size; 20 +/- 12 versus 3 +/- 9 mm Hg; 21% +/- 13% versus 8% +/- 8%, both p < 0.01). However, there was no difference in these variables between the Toronto valve and the aortic homograft (3 +/- 12 versus 2 +/- 10 mm Hg; 5% +/- 14% versus 2% +/- 12%, both p > 0.05), although the Toronto valves (normalized to body surface area) were larger than the aortic homografts (14.4 +/- 1.9 versus 12.6 +/- 1.8 mm/m2, p < 0.01). There was no significant difference in left ventricular stroke volume index or stroke work index in the systemic circulation, either between stentless and stented valves or between aortic homografts and Toronto valves, although the cross-clamp time required to insert a stentless valve was 20 minutes longer than that for a stented valve.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of valve substitute on changes in left ventricular function and hypertrophy after aortic valve replacement.

BACKGROUND: Residual left ventricular hypertrophy adversely affects long-term outcome after aortic valve replacement. A stentless biological valve in the aortic position has been shown to offer a better hemodynamic profile than a stented one. However, it remains to be defined whether this difference is translated into inter-mediate-term effects on left ventricular structure and function. METHODS: One hundred thirty-seven patients receiving single aortic valve replacement (52 with concomitant coronary artery bypass graft) were enrolled in this study. Ninety-eight were men, and the mean age was 68 years (range, 55 to 90 years). Of the 137 patients, 39 had an aortic homograft, 72 a Toronto stentless porcine valve, and 26 had a stented porcine or bileaflet mechanical valve, with mean valve size of 25 +/- 2.5 mm (mean +/- standard deviation). Left ventricular muscle mass and function were assessed by M-mode echocardiography performed before and 0.5, 6, 12, 24, and 36 months after operation, and recorded on paper for off-line digitizing. Peak valve prosthesis pressure gradients were quantified by continuous wave Doppler. RESULTS: A total of 330 echocardiograms obtained during this study were adequate for computer digitizing. Clinical data, preoperative left ventricular function, and hypertrophy were similar between the three groups. Significant improvement in left ventricular function and major regression of left ventricular hypertrophy had occurred in the entire population by 6 months after operation. Multivariate analysis of variance showed that patients with previous aortic regurgitation had a larger left ventricular cavity size (p < 0.001) and greater mass index (p = 0.001) postoperatively than those with previous aortic stenosis. In addition, peak valvular gradient was lower (p < 0.001), mass index less (p < 0.001), and left ventricular function more normal both systolic, by a greater peak velocity of dimension shortening (p = 0.05) and wall thickening (p = 0.002), and diastolic, by a greater peak velocity of dimension lengthening (p = 0.046), with an aortic homograft or stentless porcine valve compared with a mechanical or stented biological valve. There was no significant difference in peak valve gradient, left ventricular mass index, or function between the aortic homograft and the stentless porcine valve. Age, sex, and concomitant coronary artery bypass graft, as well as aortic cross-clamp time, cardioplegia method, and valve size all proved to be insignificant determinants of postoperative left ventricular hypertrophy or function. CONCLUSIONS: In the first 2 years after implantation, the superior hemodynamic performance of aortic homograft and stentless porcine valve appears to result in more extensive regression of ventricular hypertrophy and greater improvement of left ventricular function than occurs with a mechanical or stented biological valve. These findings encourage the use of a stentless biological valve in older patients requiring aortic valve replacement, and a larger scale long-term randomized study of stentless versus stented biological valve or mechanical valve seems warranted.

Early changes in the time course of myocardial contraction after correcting aortic regurgitation.

BACKGROUND: Correcting aortic regurgitation causes significant changes in left ventricular loading conditions, but few observations have been made intraoperatively of early effects on myocardial function. METHODS: We studied 18 patients (mean age, 59+/-12 years; 14 men) in whom aortic regurgitation was corrected with a stentless biologic valve. Overall left ventricular function was studied by thermodilution cardiac output, ventricular filling pressure, and systemic arterial pressure. Regional myocardial function was assessed from intraoperative transesophageal M-mode echocardiography and high fidelity ventricular pressure recordings before cardiopulmonary bypass, and 0.5, 1, 3, 6, 12, and 20 hours after operation. Time course of contraction, and magnitude of left ventricular systolic wall stress, dimensional shortening, myocardial power, and stroke work were measured. RESULTS: Global hemodynamics: there was an immediate decrease in left ventricular stroke volume (58+/-31 mL versus 80+/-30 mL, p = 0.004) and stroke work index (250+/-86 mJ/m versus 401+/-198 mJ/m, p = 0.005), but systemic arterial pressure (79+/-11 mm Hg versus 65+/-10 mm Hg, p = 0.002), increased at constant heart rate and end-diastolic pressure. Regional myocardial function and timing: peak systolic wall stress, dimensional shortening rate, and myocardial power production were all unchanged with operation. However, myocardial stroke work decreased (3.0+/-1.3 mJ/cm versus 4.8+/-2.4 mJ/cm, p = 0.009), attributable to shortening of the duration of systole (475+/-91 ms versus 543+/-67 ms, p<0.001). Diastolic time increased from 34%+/-18% to 71%+/-33% of systolic pulse duration (p<0.001). CONCLUSIONS: Correcting aortic regurgitation causes an early decrease in regional and global stroke work and increases diastolic time, although systolic wall stress does not decrease immediately. These beneficial effects are achieved by reducing the duration rather than altering the peak intensity (power) of myocardial contraction.

Early changes in left ventricular anterior wall dynamics and coordination after coronary artery surgery.

OBJECTIVE: To study how asynchronous left ventricular wall motion changes early after uncomplicated coronary artery surgery. DESIGN: A prospective study done before, and at 0.5, 1, and 3 hours after coronary artery grafting, with intraoperative transoesophageal cross sectional guided M mode echocardiograms, high fidelity left ventricular pressure, and thermodilution cardiac output measurements. The extent and velocity of left ventricular anterior wall thickening were measured, along with regional work and power production. Abnormal thickness changes during the isovolumic periods were detected, and their effect on energy transfer quantified as cycle efficiency. SETTING: Tertiary referral cardiac centre. PATIENTS: 25 patients with a history of chronic stable angina, mean (SD) age 60 (9) years with three vessel coronary artery disease, undergoing uncomplicated coronary artery bypass grafting. RESULTS: 4 patients had primary incoordination, as shown by wall thinning during isovolumic contraction and delayed onset of thickening (group A), and nine had premature thickening due to incoordination elsewhere (group B). The extent (thickening fraction 43 (12)% v 73 (19)%) and velocity (1.7 (0.4) v 2.5 (0.6) cm/s) of thickening were reduced in group A v group B (P < 0.001), as were regional stroke work (2.2 (0.8) v 3.3 (0.4) mJ/cm2) and peak power production (19 (5) v 32 (7) mW/cm2), P < 0.05. In group A, these values all increased significantly within 30 minutes of operation. In group B, the extent of wall thickening and peak power production were unaffected by surgery, though cycle efficiency and regional stroke work both improved by 30 minutes v before operation (73 (9)% v 61 (8)%, 4.5 (0.9) v 3.3 (0.4) mJ/cm2, P < 0.01). Surgery had no consistent effect on left ventricular cavity size, shortening fraction, or cardiac output in either group. CONCLUSIONS: Even in the absence of evidence of overt ischaemia, major disturbances of ventricular synchrony--both regional and generalised--are present in patients with a history of chronic stable angina requiring coronary artery bypass grafting. They regress within 30 minutes of revascularisation, suggesting that they are the direct result of coronary stenosis.

Effects of incoordination on left ventricular force-velocity relation in aortic stenosis.

OBJECTIVE: Tension development is often incoordinate in the hypertrophic left ventricle (LV). The present study aimed to elucidate the possible effects of incoordination on standard LV force-velocity relations in patients with aortic stenosis (AS). DESIGN: Prospective study during aortic valve replacement with transoesophageal cross sectionally guided M mode echocardiogram, combined with high-fidelity LV pressure recorded by pressure transducer tip catheter, and thermodilution cardiac output. SETTING: Tertiary cardiac referral centre. PATIENTS: 37 patients (mean (SD) age 63 (12)) years were studied before and 20 hours after aortic valve replacement. MAIN OUTCOME MEASURES: LV function was assessed regionally by peak velocity of circumferential fibre shortening (peak Vcf), mean systolic wall stress, and peak myocardial power; and globally by LV stroke work index. LV coordination was quantified as cycle efficiency, derived from LV pressure-dimension loop (lower normal limit > or = 76%). RESULTS: 22 patients with a coordinate LV had significantly higher peak Vcf (1.85 (0.47) v 1.46 (0.64) s-1) peak myocardial power (20.8 (8.5) v 12.0 (6.1) mW.cm-3) and global stroke work index (440 (155) v 325 (150) mJ.m-2) than those of 15 patients with an incoordinate ventricle, all P < 0.05; though there was no significant difference in LV end diastolic dimension, mean systolic wall stress, LV mass index, or the incidence of coronary artery disease (P > 0.05, respectively). Furthermore, when contraction was coordinate, mean systolic circumferential wall stress correlated inversely with peak Vcf (r = - 0.71) and positively with peak myocardial power (r = 0.83), both P < 0.01. When contraction was incoordinate, these correlations did not apply; instead peak Vcf (r = 0.65) and peak myocardial power (r = 0.73) both correlated positively with cycle efficiency (P < 0.02 and 0.01, respectively). By 20 hours after surgery, values of cycle efficiency, peak Vcf, and myocardial power were indistinguishable in the previously coordinate and incoordinate groups. CONCLUSIONS: In aortic stenosis, incoordination causes a fall in LV peak Vcf proportional to the increase in systolic wall stress, and thus modifies the standard LV force-velocity relation to mimic depressed contractility. However, incoordination and subsequent ventricular dysfunction were largely reversible once the aortic stenosis had been relieved.

Effects of acute coronary occlusion and previous ischaemic injury on left ventricular wall motion in humans.

OBJECTIVE: To assess the acute effects of single and repeated coronary artery occlusions, during percutaneous transluminal coronary angioplasty (PTCA), on left ventricular long axis function in patients with stable and unstable angina. DESIGN: Prospective examination of ventricular systolic and diastolic long axis function using M mode echocardiography and transmitral Doppler in patients with significant coronary artery stenosis and either stable or unstable angina, during routine PTCA. SETTING: A tertiary referral centre for heart disease with cardiac catheterisation and echocardiographic facilities. SUBJECTS: 36 patients, age (SD) 60 (8) years, with significant coronary artery disease undergoing PTCA (mean duration 100-130 seconds) to the left anterior descending coronary artery (LAD) in 18 patients, native LAD or its vein graft in eight, and right coronary artery in 10. Controls were 21 normal subjects, age 58 (11) years. RESULTS-AT BASELINE: in systole, total long axis excursion was reduced at septal, posterior, and right sites in patients with LAD disease, at right site in those with vein grafts, and at septal and right sites in patients with right coronary artery disease. Peak shortening rate was often reduced in all patients and onset of shortening delayed with respect to the Q wave in patients with LAD disease. In diastole, onset of lengthening was always delayed, peak lengthening rate reduced, and relative A wave amplitude increased in all patients. There was a consistent abnormal shortening of the long axis during the isovolumic relaxation period in the 14 patients with unstable angina, not seen in the others. Transmitral A wave velocity was also increased and the onset of E wave delayed with respect to A2. At first balloon inflation: the extent of pre-existing systolic and particularly diastolic abnormalities consistently increased in patients with LAD or right coronary artery occlusion. This was associated with further delay in the onset of the transmitral Doppler E wave as its peak velocity fell and E/A ratio increased. In unstable angina, balloon inflation caused minor changes only in systolic function and no change in diastolic function. At second balloon inflation: systolic changes were the same as with the first inflation, while diastolic changes were attenuated by 10-15%. CONCLUSIONS: In stable angina intracoronary balloon inflation aggravated pre-existing systolic and diastolic abnormalities in the territory of the occluded vessel, indicating the dependence of both on coronary flow. In unstable angina balloon inflation caused only minor deterioration in systolic function, and diastolic changes-including the characteristic abnormal shortening during isovolumic relaxation-were unaffected. Thus resting abnormalities of left ventricular function in unstable angina are effectively dissociated from acute changes in coronary flow. Overall, the severity of systolic disturbances was unaltered by a second balloon inflation, but diastolic disturbances were attenuated by 10-15%, compatible with ischaemic preconditioning or recruitment of collaterals.