Right ventricular stunning in inferior myocardial infarction.

AIM: To assess right ventricular (RV) function in patients with inferior myocardial infarction (IMI) and to observe changes following thrombolysis. BACKGROUND: RV dysfunction occurs in 30% of patients with IMI. The extent of such involvement and its potential, recovery has not been determined. METHODS: We studied 30 patients with acute IMI (age 56+/-12 years), on admission, day 7 and day 30 post thrombolysis. No patient had clinical signs of RV failure. RV segmental function was assessed from free wall long axis and global function from filling and ejection velocities. Values were compared with 15 age-matched controls. RESULTS: On admission, RV long axis amplitude, systolic and diastolic velocities were depressed (2.09+/-0.39 vs 2.6+/-0.3 cm, 8.18+/-1.8 vs 10.0+/-2.0 cm/s and 6.9+/-2.7 vs 10.0+/-2.5 cm/s, p<0.01 for all) and global function impaired; reduced Z ratio (0.85+/-0.07 vs 0.9+/-0.04, p<0.01), raised Tei index (0.49+/-0.26 vs 0.3+/-0.1, p<0.001) and prolonged t-IVT (8.16+/-3.9 vs 4.8+/-2 s/m, p<0.01) compared to controls. After thrombolysis, RV long axis amplitude (2.28+/-0.3 cm, p<0.05), systolic velocity (10.0+/-2.7 cm/s, p<0.01), early diastolic velocity (8.3+/-2.16, p<0.05), Z ratio (0.9+/-0.05, p<0.01), Tei index (0.34+/-0.17, p<0.01) and t-IVT (6.2+/-2.7 s/m, p<0.05) all normalised at day 30. Only 4 (13%) patients remained with RV long axis amplitude and one with t-IVT and Tei index values outside the normal 95% CI at day 30. RV inflow diameter and tricuspid regurgitation did not change. CONCLUSION: In IMI, RV segmental and global functions are acutely impaired, and recover in 87% of patients following thrombolysis. In the absence of clear evidence for RV infarction the disturbances in the remaining 13% may represent stunned myocardium that may demonstrate delayed recovery.

Medium-term outcome of Toronto aortic valve replacement: single center experience.

BACKGROUND AND AIMS: Long-term competence of any aortic prosthesis is critical to its clinical durability. Bioprosthetic valves, and in particular the stentless type have been proposed to offer superior haemodynamic profiles with consequent potential for superior left-ventricular mass regression. These benefits however are balanced by the potential longevity of the implanted valve. The aims of this study were to assess medium-term Toronto aortic valve function and its effect on left-ventricular function. METHODS: Between 1992 and 1996 86 patients underwent Toronto aortic valve replacement for aortic valve disease and were followed up annually. Prospectively collected data was analyzed for all patients where detailed echocardiographic follow-up was available. Echocardiographic studies were analyzed at 2+/-0.6 and 6+/-1.4 years after valve replacement. Data collected included left-ventricular systolic and diastolic dimensions, fractional shortening and left-ventricular mass. In addition, data on aortic valve and root morphology, peak aortic velocities, time velocity integral, stroke volume and the mechanism of valve failure where relevant, were also collected. RESULTS: Complete echocardiographic data were available for eighty-four patients, age 69+/-9 years, 62 male. Additional coronary artery bypass grafting was performed in 38% of patients. Twelve (14%) valves had failed during follow-up, 7 (8%) requiring re-operation. Valve failure was associated with morphologically bicuspid native aortic valve (9/12), and progressive dilatation of the aortic sinuses, sino-tubular junction and ascending aorta (11/12). Left-ventricular mass index remained high (184+/-75 g/m(2)) and did not continue to regress between early and medium-term follow-up (175.8+/-77 g/m(2)). CONCLUSIONS: Although more than 90% of implanted Toronto aortic valves remained haemodynamically stable with low gradient at medium-term follow-up, young age and larger aortic dimensions in patients with valve failure suggest better outcome if used in the elderly with normal aortic root geometry.

Ventricular endocrine and mechanical function following thrombolysis for acute myocardial infarction.

OBJECTIVE: The objective of this study was to assess natriuretic peptide release following acute myocardial infarction, and its relationship with ventricular function. METHODS: A total of 44 patients with acute myocardial infarction were studied; 13 anterior, age (57+/-12 years) and 31 inferior, age (58+/-12 years). Peptide levels and left ventricular function by echocardiography were assessed at admission and on days 7 and 30 after thrombolysis. Healthy volunteers (n=21) served as controls. RESULTS: Atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) levels rose from admission to day 7 (p=0.002). While ANP remained elevated at day 30 in both groups, BNP levels fell in patients with anterior myocardial infarction (p=0.03). Left ventricular fractional shortening was reduced at admission in the two groups (p=0.01) but returned towards normal in 7 days (p=0.001) in inferior myocardial infarction and in 30 days in anterior myocardial infarction (p=0.02). Left ventricular long axis amplitude was universally reduced at admission (p=0.01) and remained abnormal at day 30 (p=0.01) in both groups. At day 7, BNP and ANP levels inversely correlated with long axis amplitude of lateral wall in anterior myocardial infarction; (r=-0.7, p=0.01). BNP correlated inversely with fractional shortening in anterior myocardial infarction (r=-0.7, p=0.01) at day 30. CONCLUSION: The elevated peptide levels at 7 days post-myocardial infarction correlate with reduced mechanical activity of the adjacent noninfarcted segment. Natriuretic peptides release seem to be related to failure of compensatory hyperdynamic activity of the noninfarcted area rather than directly from the injured myocardial segments.

Dobutamine stress-induced ischemic right ventricular dysfunction and its relation to cardiac output in patients with three-vessel coronary artery disease with angina-like symptoms.

We investigated markers of ischemic dysfunction and their relation to overall right ventricular (RV) performance during dobutamine stress echocardiography in patients who had coronary artery disease. Thirty-three patients (58 +/- 10 years old) who had 3-vessel coronary artery disease were compared with 17 age-matched controls (58 +/- 11 years old). RV long-axis amplitude (M mode), systolic and diastolic myocardial tissue Doppler velocities, and filling and ejection velocities were measured, and cardiac output (CO) was calculated at rest and during peak stress. There was no difference in RV size (inlet dimension <3.5 cm), RV systolic long-axis amplitude, systolic and diastolic velocities, peak early/late diastolic velocity ratio, and RV CO between patients and controls at rest. During stress, RV systolic long-axis amplitude increased in controls (from 24 +/- 6 to 30 +/- 5 mm) and CO increased significantly (from 4.9 +/- 1.2 to 12.5 +/- 2.1 L/min, p <0.001 for the 2 items). In contrast, RV amplitude did not change with stress in patients (from 24 +/- 5 to 22 +/- 6 mm, p = NS), and the stress-increment in CO was augmented (from 4.2 +/- 1.2 to 8.3 +/- 2.0 L/min, p <0.001 vs control stress increment). Failure to increase RV systolic amplitude >2 mm was 79% sensitive and 88% specific for detecting ischemic RV dysfunction, and there was a close correlation between stress-induced change in RV systolic amplitude and change in CO in patients (r = 0.56, p <0.001). Early diastolic velocity increased in controls (from 10.8 +/- 3.2 to 13.1 +/- 3.6 cm/s, p <0.01) but did not change in patients (from 11.5 +/- 3.7 to 11.3 +/- 4.8 cm/s, p = NS). RV shortening after ejection did not appear in any control subject but did develop in 8 of 33 patients, thus contributing to the decrease in RV peak early/late diastolic velocity ratio in patients (from 1.1 +/- 0.3 to 0.76 +/- 0.4, p <0.001) compared with that in controls (1.3 +/- 0.3 to 1.0 +/- 0.2, p <0.001). In conclusion, markers of RV dysfunction are not related to left ventricular wall motion score index or long-axis changes with stress.

Opposite effects of coronary artery disease and hypertrophic cardiomyopathy on left ventricular long axis function during dobutamine stress.

BACKGROUND: The mechanism for reduced early diastolic long axis lengthening velocity in hypertrophic cardiomyopathy (HCM) is not known. METHODS: We measured simultaneous septal long axis amplitude and early lengthening velocity in 23 patients with HCM, 23 normal subjects and 22 patients with coronary artery disease (CAD) of left anterior descending artery. RESULTS: Resting amplitude and lengthening velocity were reduced in HCM 0.9+/-0.2 cm, 3.5+/-1.9 cm/s but equally in CAD 1.0+/-0.3 cm, 4.1+/-2.5 cm/s vs. 1.3+/-0.2 cm, 6.3+/-1.7 cm/s in normals, p < 0.01 for both vs. normal. With dobutamine stress, lengthening velocity increased by 2.7+/-1.9 cm/s (p < 0.001) in normals, by 2.8+/-2.5 cm/s (p < 0.001) in HCM but not in patients with CAD 0.5+/-2.1, p = NS. Increment in total long axis amplitude was subnormal in CAD and HCM. However, increment in lengthening velocity was higher with stress for corresponding change in amplitude in HCM compared with CAD (chi2) = 16.5, p < 0.001). An increase in early lengthening velocity by 2 cm/s was 77% sensitive and 70% specific in discriminating between HCM and CAD. Post-ejection shortening developed or worsened in all CAD patients indicating ischemia but not in any with HCM. CONCLUSIONS: Reduced peak early lengthening velocity is not specific for HCM but also occurs in CAD. Unlike CAD, lengthening velocity increases in HCM with stress and there is no aggravation of post-ejection shortening, suggesting that the abnormal relaxation is not due to subendocardial ischemia in HCM. The greater recoil velocity per unit deformation in HCM compared with CAD, indicates elastic mechanism with increased passive muscle stiffness due to fibrosis or fibre disarray.

Systole-diastole mismatch in hypertrophic cardiomyopathy is caused by stress induced left ventricular outflow tract obstruction.

BACKGROUND: Pharmacological stress is used to assess the degree of left ventricular (LV) subvalvular gradient in patients with hypertrophic cardiomyopathy (HCM), but there is little information about associated physiological changes. METHODS: Echocardiography-Doppler ultrasound scanning measurements in 23 patients with HCM and 23 control subjects of similar age were studied at rest and at the end point of dobutamine stress. RESULTS: In patients, the systolic time was normal at rest, but increased abnormally with stress. In patients, the total isovolumic contraction time failed to shorten, and the total ejection time increased abnormally. Changes in total ejection time correlated with an increase in peak subvalvular gradient in control subjects and patients (r = 0.52 and r = 0.66, respectively; P <.01 for both). In patients, the diastolic time was normal at rest, but shortened abnormally with stress. In patients, the isovolumic relaxation time fell abnormally, as did the filling time. Mitral E wave acceleration and left atrium size were unchanged with stress in control subjects, but consistently increased in patients with HCM, which indicates an increased early diastolic atrioventricular pressure gradient. CONCLUSION: In HCM, systolic period increases abnormally with stress. This is not because of a loss of inotropy, but is directly related to the degree of LV outflow tract obstruction. As a result, the diastolic period fails to increase, reducing the time available for coronary flow, the LV filling pattern is modified, and the diastolic atrioventricular pressure gradient increases. These changes may contribute to symptom development and suggest why reducing LV outflow tract obstruction per se may be therapeutically useful in HCM.

The effect of the Q wave infarct on left ventricular electromechanical function.

OBJECTIVE: To assess the nature of left ventricular (LV) electrical and mechanical dysfunction in Q compared to non-Q anterior myocardial infarction (MI). SUBJECTS: We used ECG and echocardiography to study 54 unselected patients, age 57+/-15 years, 32 male, with old (>6 months after) anterior MI (39 Q and 15 non-Q), confirmed by enzyme rise and regional wall motion abnormality, and compared them with 21 normals of similar age. METHODS: Analysis of resting LV minor and long axis function and 12-lead surface electrocardiogram. RESULTS: Only 10% of normals did not have a normal septal Q wave compared with 46% of non-Q wave MI and 84% Q wave MI (P<0.001). All patients with Q wave MI had a scarred anteroseptal wall but none of the non-Q wave MI. LV minor axis dimensions were increased only with Q wave MI: 6.0 +/- 0.9 vs. 4.9 +/- 0.5 cm at end-diastole and 4.5 +/- 1.1 vs. 3.3 +/- 0.5 cm at end-systole and fractional shortening was reduced 27 +/- 8 vs. 33 +/- 3% (P<0.001 for all). Total left ventricular long axis amplitude of motion was reduced at the left, septal and posterior sites only in Q wave MI but was not different from controls in non-Q wave MI. The onset of long axis shortening was delayed by 20 ms at the left and septal sites in non-Q wave MI and by an additional 20 ms at the three sites in Q wave MI. Peak long axis shortening rate was reduced in the two patient groups, with the same distribution as post-ejection shortening (greater than 1 mm), which occurred in 21% of patients with non-Q wave MI and 76% of patients with Q wave MI (P<0.001). In diastole, the onset of long axis lengthening was delayed by 20 ms at the left and septal sites in non-Q wave MI and at the three sites in Q wave MI (P<0.001). Peak long axis lengthening rate was reduced with a similar distribution in the two patient groups. CONCLUSION: Patients with Q wave MI have an increased LV dimension and reduced FS, whereas patients with non-Q wave MI appear to have morphologically normal LV minor axis dimensions and fractional shortening apart from the anterior wall hypokinesis. In the latter, however, long axis function shows significant systolic and diastolic disturbances affecting the anteroseptal and lateral walls. The absence of conduction disturbances in non-Q wave MI suggests intrinsic myocardial dysfunction that may be reversible.

Evidence for rheumatic valve disease in patients with severe tricuspid regurgitation long after mitral valve surgery: the role of 3D echo reconstruction.

BACKGROUND AND AIM OF THE STUDY: Although severe tricuspid regurgitation (TR) is a well-recognized, long-term complication of rheumatic mitral valve replacement that impairs the functional results of surgery, its exact basis remains unclear and its management is unsatisfactory. The study aim was to obtain a detailed assessment of tricuspid valve morphology and function using 2D transesophageal echocardiography (TEE) with 3D reconstruction, and to determine long-term clinical outcome in patients after surgery for rheumatic mitral valve disease. METHODS: A total of 42 patients (mean age 50 +/- 10 years) was followed up; 39 patients had mitral replacement and three had valvotomy. Thirty patients had developed impaired exercise tolerance, fluid retention and echocardiographic evidence of severe TR at 8.2 +/- 2.6 years after surgery; the remainder had mild regurgitation. RESULTS: Follow up showed greater mortality in the severe TR group, with approximately 50% survival at 60 months after diagnosis compared with mild TR. None of the patients with severe TR had a dysfunctional mitral prosthesis. In these patients, transthoracic echo-Doppler showed enlarged right atrium and right ventricle, a mean transtricuspid retrograde pressure drop of 15 +/- 4 mmHg and apparently normal leaflet anatomy. Twenty patients (15 with severe TR) underwent a TEE and 3D reconstruction study for further evaluation. Abnormal leaflet anatomy was demonstrated in all patients with severe TR, with restricted leaflet motion in 10, leaflet shortening and thickening in the remainder, and dilatation of tricuspid valve annular insertion suggestive of rheumatic involvement. Although diastolic transtricuspid velocities were increased (peak flow 0.8 +/- 0.1 m/s) in these patients due to increased stroke volume, significant tricuspid stenosis was present in only two cases (mean gradient 4 and 3 mmHg respectively). Histopathology confirmed the presence of leaflet vascularization and extensive fibrosis in two patients who underwent tricuspid valve replacement. CONCLUSION: Rheumatic leaflet involvement contributes to severe TR occurring long after mitral valve replacement, though overt stenosis is uncommon. Knowledge of the structural basis of this condition may thus improve its long-term management, possibly with early tricuspid valve repair.

The effect of the localization of Q wave myocardial infarction on ventricular electromechanics.

BACKGROUND: The exact location of a Q wave myocardial infarction has an important effect on overall left ventricular function. OBJECTIVES: To assess the effect of localization of Q wave infarction on left ventricular minor and long axis function, with particular reference to electromechanical disturbances. METHODS: We studied 72 patients with Q wave myocardial infarction; 35 anterior, age 61+/-15 years and 37 inferior, age 62+/-12 years. ECG intervals were automatically measured by Hewlett-Packard Pagewriter and LV dimension and filling velocities studied by transthoracic echocardiography and simultaneous phonocardiogram. Findings were compared with 21 controls of similar age. RESULTS: Heart rate and all ECG intervals were similar in the two patient groups and controls. QRS axis was more to the left in patients with inferior MI. Normal septal q wave was absent in lead V5 and V6 in 33/35 (94%) patients with anterior MI and in only 3/37 (8%) with inferior MI, p<0.001. LV minor axis dimensions were enlarged vs. normal (p<0.001) in the two patient groups and to a greater extent in anterior MI compared with inferior MI, p<0.05. Isovolumic relaxation time was prolonged only in-patients with an inferior MI, p<0.01. Long axis amplitude was globally reduced (p<0.001) in the two patient groups as were shortening and lengthening velocities (p<0.001). The onset of septal long axis shortening with respect to the q wave was delayed by 30 and 40 ms in inferior MI and anterior MI and that of lengthening with respect to A2 by 20 and 30 ms, respectively, compared to normal (p<0.001 for both). Post ejection shortening was localized to the septal long axis in 32/35 patients with anterior MI but was generalized involving all three LV long axes in inferior MI, p<0.001. Transmitral Doppler flow velocities and the frequency of mild mitral regurgitation were similar in the two groups. CONCLUSION: These results confirm a close association between anterior Q wave infarction, septal incoordination and absent septal q waves. The global incoordinate long axis behaviour in inferior Q wave MI may be due to significant papillary muscle dysfunction, and results in significant shape change in early diastole. This disturbance in electromechanical behaviour might play an important role in the differing outcomes between the two different sites of myocardial infarction.