Tissue Doppler echocardiography is a novel technique that can be used to diagnose right ventricular (RV) systolic dysfunction. Until recently, there have been no data on the influence of tissue Doppler-derived RV systolic dysfunction on exercise capacity after inferior (posterior) myocardial infarction (MI). We studied 90 consecutive patients (76% men, mean age 61 ± 10 years) with first inferior ST-segment elevation MI and left ventricular ejection fraction ≥45%. RV systolic dysfunction was defined as RV systolic myocardial velocity <11.5 cm/s at the basal segment of the RV free wall assessed by pulse tissue Doppler. Patients were categorized as with or without RV systolic dysfunction (RV systolic myocardial velocity 9.34 ± 1.36 and 13.74 ± 1.58 cm/s, respectively). A cardiopulmonary exercise test was performed before or soon after discharge (day 14 ± 10). Patients with RV systolic dysfunction had lower oxygen consumption assessed as percent predicted oxygen uptake in liters per minute and milliliters per kilogram per minute at their anaerobic threshold (61 ± 11% vs 69 ± 17%, p = 0.007; 53 ± 12% vs 61 ± 19%, p = 0.012, respectively) and at peak exercise (71 ± 12% vs 83 ± 16%, p = 0.0001; 62 ± 14% vs 74 ± 21%, p = 0.002, respectively). Multivariate regression analysis revealed that the following independent factors negatively influenced exercise capacity: RV systolic dysfunction, female gender, age, lower body mass index, current smoking, and maximal troponin I concentration. In conclusion, we found decreased exercise capacity in patients with systolic RV dysfunction assessed by pulse tissue Doppler in patients with inferior (posterior) wall acute MI despite preserved left ventricular function.
Tissue Doppler echocardiography is a novel technique that can be used to diagnose right ventricular (RV) systolic dysfunction. This has also been confirmed in patients with acute myocardial infarction (MI). Decreased exercise capacity is an established marker of poor prognosis in patients with coronary artery disease or chronic heart failure and in the general population. Until recently, there have been no published data on the influence of tissue Doppler-derived RV systolic dysfunction on exercise capacity after inferior (posterior) MI. The aim of this study therefore was to assess influence of tissue Doppler-derived RV systolic dysfunction on exercise capacity in patients after inferior (posterior) wall acute MI.
Methods
We prospectively enrolled consecutive patients admitted from January 2007 through November 2009 to the department of cardiology, Postgraduate Medical School, Grochowski Hospital in Warsaw, Poland with first ST-segment elevation inferior MI up to 48 hours from onset of symptoms. All included patients were treated by primary percutaneous coronary angioplasty. ST-segment elevation inferior MI was diagnosed by the presence of chest pain lasting >30 minutes together with electrocardiographic criteria (ST-segment elevation ≥1 mm in 2 contiguous lead II, III, or aVF) and an increase in troponin I. In cases with ST-segment depression ≥0.5 mm in 2 contiguous leads V 1 to V 4 , concomitant posterior MI was diagnosed. Exclusion criteria were narrow stenosis in a noninfarct-related artery not qualifying for angioplasty, previous heart failure, left ventricular (LV) systolic dysfunction (ejection fraction <45%), hemodynamically important defects of mitral or aortic valves, tricuspid or pulmonary valve stenosis, documented pulmonary hypertension, pulmonary embolism, atrial fibrillation or other rhythm disturbances complicating echocardiographic assessment, fixed left bundle branch block, technical factors that prevented meaningful echocardiography, inability to perform exercise, and refusal to give consent.
Transthoracic echocardiography with pulse tissue Doppler (VIVID 4, General Electric, Haifa, Israel) was performed in the first 48 hours after primary percutaneous coronary intervention. Echocardiographic images were recorded in standard projections. All measurements were performed according to recommendations of the American Society of Echocardiography.
The pulse tissue Doppler sample volume was placed in the middle of basal segments of the RV free wall and LV septum, lateral, inferior and anterior walls. Systolic myocardial velocity (Sm), early diastolic myocardial velocity (Em), and late diastolic myocardial velocity were recorded. Tissue Doppler echocardiographic measurements were performed during shallow respiration or end-expiratory apnea.
Patients were categorized according to their RV systolic function: those with RV systolic dysfunction (RV Sm <11.5 cm/s) and those without RV systolic dysfunction (RV Sm ≥11.5 cm/s).
LV systolic function was assessed by ejection fraction (modified Simpson rule), wall motion score index, and pulse tissue Doppler parameters at the basal segments of the left ventricle. For group comparison LV Sm values from the septal, lateral, inferior, and anterior walls were averaged. For diastolic assessment we used averaged values of LV Em from the septal and lateral walls and transmitral inflow velocities.
Physical activity was assessed as low, moderate, or high according to activity and loads in the 1 week before MI.
A symptom-limited cardiopulmonary treadmill stress test with a Schiller Cardiovit CS-200 (Schiller, Baar, Switzerland) and an Ergo Spiro adapter (Ganshorn, Niederlauer, Germany) was performed at the same time of day (11 a.m. to 1 p.m. ) before or soon after hospital discharge. A modified Bruce protocol was used in all cases. Oxygen consumption, carbon dioxide production, and ventilation during exercise were analyzed breath by breath. A patient’s exertion score ≥8 (on the 10-point Borg scale) or respiratory exchange ratio >1.0 was taken to indicate maximal effort. All exercise tests were performed according to American College of Cardiology/American Heart Association guidelines.
Oxygen consumption at peak exercise and at anaerobic threshold and percent predicted maximal oxygen uptake were used as exercise capacity parameters. Values are expressed as liters per minute and as milliliters per kilogram of body weight per minute. Predicted values of maximal oxygen uptake (liters per minute) were calculated from the following equations: for men ([50.72 − 0.372 × age in years] × predicted body weight in kilograms)/1,000; for women ([22.78 − 0.17 × age in years] × [predicted body weight in kilograms + 43])/1,000. Predicted body weight was calculated from the Broca index. Anaerobic threshold was assessed using the V-slope method. Other exercise parameters analyzed were exercise duration, heart rate exercise acceleration, heart rate at peak exercise, and blood pressure at peak exercise.
Continuous variables are expressed as mean ± SD, number (percentage), or median (25th to 75th interquartile range) depending on the distribution of the variable. Independent parameters were assessed using Student’s t test and Kruskal–Wallis test for parametric values and chi-square test for categorical variables. Normal distribution was checked by Shapiro–Wilke test. Differences were recognized as statistically significant at a p value <0.05. We used a regression model to analyze the following variables for potential influences on exercise capacity: gender, age, body mass index, physical activity before MI, diabetes mellitus/impaired glucose tolerance, hypertension, smoking, LV ejection fraction, wall motion score index, maximal troponin concentration, RV Sm, RV Em, LV Sm, LV Em, and ratio of early transmitral inflow velocity to LV Em. Parameters with no influence on exercise capacity were removed from the model (p >0.1). Variables are presented with coefficient beta values and 95% confidence intervals. All data analyses were performed using STATA 9.0 (STATA Corp., College Station, Texas).
The bioethical committee of the Postgraduate Medical School in Warsaw approved the protocol. All patients gave written informed consent at time of enrollment. The study met the requirements of the Helsinki Convention current at the time.
Results
Ninety-nine consecutive patients fulfilled the inclusion criteria. Nine patients were excluded from analysis because 3 died before discharge, 2 refused to perform the cardiopulmonary stress test, 1 developed decompensated heart failure, 1 had a hypertensive response at exercise, 1 developed ventricular arrhythmia, and 1 developed intermitted claudication. Thus 90 eligible patients were enrolled. The group with RV systolic dysfunction was comprised of 49 patients (80% men, mean age 60 ± 9 years). The group without RV systolic dysfunction was comprised of 41 patients (71% men, mean age 61 ± 12 years). Concomitant posterior MI was discovered in 27 patients (55%) and 21 patients (51%) in the groups with and without RV dysfunction. Demographic and in-hospital clinical characteristics are presented in Tables 1 and 2 .
| Variable | All (n = 90) | RV Dysfunction | p Value | |
|---|---|---|---|---|
| Yes | No | |||
| (n = 49) | (n = 41) | |||
| Age (years) | 61 ± 10 | 60 ± 9 | 61 ± 12 | 0.925 |
| Men | 68 (76%) | 39 (80%) | 29 (71%) | 0.330 |
| Body mass index (kg/m 2 ) | 27.0 ± 3.7 | 27.9 ± 4.0 | 27.3 ± 3.5 | 0.366 |
| Diabetes mellitus or impaired glucose tolerance | 19 (21%) | 13 (27%) | 6 (15%) | 0.168 |
| Hypertension ⁎ | 56 (62%) | 32 (65%) | 24 (59%) | 0.509 |
| Hyperlipidemia † | 63 (70%) | 32 (65%) | 31 (76%) | 0.288 |
| Chronic obstructive pulmonary disease/asthma | 7 (8%) | 3 (6%) | 4 (10%) | 0.521 |
| Former smoker ‡ | 21 (23%) | 12 (24%) | 9 (22%) | 0.776 |
| Current smoker | 53 (59%) | 29 (59%) | 24 (59%) | 0.950 |
| Physical activity before myocardial infarction | ||||
| High | 24 (27%) | 12 (24%) | 12 (29%) | 0.609 |
| Moderate | 47 (52%) | 26 (53%) | 21 (51%) | 0.861 |
| Low | 19 (21%) | 11 (22%) | 8 (20%) | 0.733 |
⁎ Blood pressure ≥140/90 mm Hg or treatment with antihypertensive medication.
† Low-density lipoprotein cholesterol ≥130 mg/dl.
| Variable | All (n = 90) | RV Dysfunction | p Value | |
|---|---|---|---|---|
| Yes | No | |||
| (n = 49) | (n = 41) | |||
| Time from myocardial infarction onset to percutaneous coronary intervention (min) ⁎ | 215 (145–445) | 220 (154–485) | 195 (130–430) | 0.260 |
| Culprit lesion in proximal right coronary artery | ||||
| Segment 1 | 24 (27%) | 19 (39%) | 5 (12%) | 0.004 |
| Segment 2 | 35 (39%) | 18 (37%) | 17 (41%) | 0.646 |
| Culprit lesion in distal right coronary artery | ||||
| Segment 3 | 16 (18%) | 5 (10%) | 11 (27%) | 0.399 |
| Segment 4 | 3 (3%) | 1 (2%) | 2 (5%) | 0.455 |
| Culprit lesion in circumflex artery | 12 (13%) | 6 (12%) | 6 (14%) | 0.739 |
| Thrombolysis In Myocardial Infarction 3 flow in culprit lesion after percutaneous coronary intervention | 75 (83%) | 40 (82%) | 35 (85%) | 0.636 |
| Glycoprotein IIb/IIIa antagonists | 76 (84%) | 42 (86%) | 34 (83%) | 0.716 |
| Killip class IV | 3 (3%) | 3 (6%) | 0 (0%) | 0.107 |
| Thrombolysis In Myocardial Infarction risk score | 2.71 ± 1.98 | 2.98 ± 2.13 | 2.39 ± 1.80 | 0.162 |
| Troponin I maximal concentration (ng/ml) | 40.2 ± 37.0 | 46.9 ± 42.9 | 32.3 ± 26.9 | 0.062 |
| Medication on day of exercise test | ||||
| Acetylsalicylic acid | 90 (100%) | 49 (100%) | 41 (100%) | |
| Clopidogrel | 90 (100%) | 49 (100%) | 41 (100%) | |
| β Blockers | 86 (96%) | 47 (96%) | 39 (95%) | 0.855 |
| Angiotensin-converting enzyme inhibitors | 85 (94%) | 46 (94%) | 39 (95%) | 0.797 |
| Statins | 90 (100%) | 49 (100%) | 41 (100%) | |
| Diuretics | 13 (14%) | 7 (14%) | 6 (15%) | 0.862 |
| Calcium channel blockers | 10 (11%) | 6 (12%) | 4 (10%) | 0.708 |
Mean values of RV Sm in the groups with and without RV systolic dysfunction were 9.34 ± 1.36 and 13.74 ± 1.58 cm/s. Other echocardiographic parameters are listed in Table 3 . We found positive correlations between RV Sm and other RV systolic function parameters such as fractional area change (n = 90, r = 0.65, p <0.000 01) and tricuspid annulus plane systolic excursion (n = 89, r = 0.7, p <0.000 01).
| Variable | RV Dysfunction | p Value | |
|---|---|---|---|
| Yes | No | ||
| (n = 49) | (n = 41) | ||
| Right ventricular end-diastolic dimension (cm) | 3.3 ± 0.7 | 3.1 ± 0.5 | 0.119 |
| Right ventricular fractional area change (%) | 26 ± 12 | 46 ± 10 | <0.0001 |
| Tricuspid annulus plane systolic excursion (mm) | 14 ± 2 (n = 29) | 21 ± 3 (n = 24) | <0.0001 |
| Right ventricular early diastolic myocardial velocity (cm/s) | 7.74 ± 2.55 | 10.24 ± 3.34 | 0.0004 |
| Right atrial dimension (cm) | 3.6 ± 0.6 | 3.5 ± 0.5 | 0.234 |
| Inferior vena cava collapsibility (%) | 38 ± 23 (n = 41) | 51 ± 20 (n = 39) | 0.009 |
| Left ventricular end-diastolic dimension (cm) | 4.6 ± 0.5 | 4.7 ± 0.4 | 0.563 |
| Left atrial dimension (cm) | 3.7 ± 0.5 | 3.8 ± 0.6 | 0.684 |
| Left ventricular ejection fraction (%) | 56 ± 9 | 60 ± 9 | 0.085 |
| Wall motion score index | 1.75 ± 0.29 | 1.58 ± 0.18 | 0.001 |
| Left ventricular systolic myocardial velocity (cm/s) | 6.75 ± 1.44 | 7.49 ± 1.76 | 0.003 |
| Early/atrial transmitral inflow velocity ratio | 0.9 ± 0.4 | 0.9 ± 0.3 | 0.712 |
| Left ventricular early diastolic myocardial velocity (cm/s) | 7.14 ± 1.85 | 7.64 ± 1.97 | 0.169 |
| Early transmitral inflow velocity/left ventricular early diastolic myocardial velocity | 9 ± 2 | 10 ± 3 | 0.603 |
Data from exercise testing are presented in Table 4 . None of the patients had exercise limiting factors other than dyspnea and/or fatigue. Oxygen uptake parameters expressed as percent predicted values were lower at peak exercise and at the anaerobic threshold in patients with than in those without RV systolic dysfunction ( Table 5 ).
