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UNLABELLED: Little information is available regarding the determinants of systolic contractile function of the hypertrophied right ventricle (RV). The purpose of this study was to clarify the relationship between myocardial metabolism and contractile function in the hypertrophied RV due to pulmonary hypertension (PH). METHODS: Iodine-123-labeled 15-(p-iodophenyl)-3-(R,S)-methylpentadecanoic acid (BMIPP) and 99mTc-sestamibi (MIBI) SPECT were performed to calculate the RV-to-left ventricle (LV) tracer uptake ratio (RV/LV) in 21 patients with PH (6 with primary PH and 15 with chronic thromboembolic PH). The patients also underwent electron-beam CT to assess RV ejection function (RVEF) and percentage systolic wall thickening (%SWT) and right heart catheterization to measure mean pulmonary arterial pressure (mPAP). RESULTS: There were significant positive correlations between mPAP and MIBI-RV/LV (r = 0.89, p < 0.001) and between mPAP and BMIPP-RV/LV (r = 0.86, p < 0.001). However, 8 patients showed lower BMIPP-RV/LV than MIBI-RV/LV, indicating the impairment of myocardial fatty acid uptake in the RV. These patients had lower RVEF and %SWT compared to those with normal myocardial fatty acid uptake (RVEF = 28% +/- 10% compared to 40% +/- 9% and %SWT = 33% +/- 27% compared to 74% +/- 30%, respectively; p < 0.05 for both comparisons). Although mPAP did not differ between the groups, the RVEF-mPAP and %SWT-mPAP regression lines drawn from the patients with impaired myocardial fatty acid uptake were located below the lines from the patients with normal myocardial fatty acid uptake, suggesting disproportionately decreased RV myocardial contractility for a given mPAP in patients with impaired myocardial fatty acid uptake. The patients with the impaired fatty acid uptake in the RV had a significantly higher death rate (log-rank test, p < 0.05). CONCLUSION: The results from this preliminary study suggest that myocardial fatty acid uptake is impaired in the failing hypertrophied RV due to PH.
We describe the case of a 59-year-old man who developed anterior ST segment elevation and Q waves due to isolated right ventricular branch occlusion during right coronary angioplasty. Isolated right ventricular infarction was clearly demonstrated on echocardiography.
We evaluated regional right ventricular wall motion during systole in patients with surgically repaired tetralogy of Fallot (TOF) using color kinesis imaging. Color kinesis images were obtained in a subcostal sagittal view from 19 patients with repaired TOF (TOF group), aged 3 to 5 years, and 20 age-matched normal subjects (control group). For regional wall motion analysis, the endocardial motion distance and the fractional area change (FAC) were calculated for 6 segments obtained from color kinesis images. The endocardial inward excursion distances and the FACs in the upper, middle, and lower posterior segments of the TOF group were significantly greater than those of the control group (p <0.01 for each segment). The upper anterior segment showed significantly reduced inward excursion distance and FAC in the TOF group than in the control group (p <0.01, both). The dyskinetic outward excursion distances of the middle and lower posterior segments were significantly lower in the TOF group than in the control group (p <0.01, both). In the upper and middle anterior segments, the endocardial outward excursion distances were significantly higher in the TOF group than in the control group (p <0.01 and 0.05). Correlation between right ventriculographic and color kinesis measurements was excellent (y = 1.14x - 1.30, r = 0.87 for the endocardial inward excursion, and y = 1.03x +/- 0.56, r = 0.91 for the FAC). In conclusion, color kinesis is a useful method for assessing regional right ventricular wall motion. Segmental analysis of color kinesis images provides accurate, automated, and quantitative diagnosis of regional right ventricular wall motion abnormalities in patients with surgically repaired TOF.
In a series of articles the authors discuss literature data concerning epidemiology of pulmonary hypertension, modern classification; peculiarities of its pathogenesis and treatment in various diseases and conditions. In the second part they consider peculiarities of pathogenesis of pulmonary hypertension and right ventricular failure in patients with predominant involvement of left cardiac chambers. Effects of various classes of drugs used in the treatment of left ventricular heart failure including their influence on pulmonary circulation and functional state of the right ventricle are also discussed.
Predictive factors of right ventricular failure after heart transplantation are not well identified. Clinical and hemodynamic data from 20 patients who developed right heart failure were compared to those of 20 matched patients who did not experience this complication after cardiac transplantation. Preoperative systemic and pulmonary hemodynamics were comparable in the two groups. Patients with posttransplant right ventricular failure had longer waiting time (27 +/- 6 vs 16 +/- 3 weeks, mean +/- SE, P < 0.05), no regression of pulmonary hypertension (0 +/- 0.1 vs 2.3 +/- 0.3 Wood units reduction in pulmonary vascular resistance after transplantation, P < 0.01), and had been ventilated with higher levels of positive end-expiratory pressure (5 +/- 1 vs 1.5 +/- 0.5 cm H2O, P < 0.05). One-month postoperative evolution (mortality, hospital stay, radionuclide ejection fractions) was similar in the two groups. These results suggest that a lesser reversibility of pulmonary hypertension (possibly due to a longer evolution of the cardiac disease, as indicated by the longer waiting time) is the main determinant of right ventricular failure after heart transplantation.
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Type B Natriuretic Peptide (BNP) is a neurohormone that is secreted from the cardiac ventricles in response to dilatation or an increase of pressure. Right ventricle dysfunction is seen in pulmonary embolism patients, but it may be hard to diagnose. Echocardiography is the most sensitive means of diagnosis for acute right ventricle dysfunction. However, echocardiography is also limited in some ways. BNP levels may increase with right ventricle dysfunction when the patients is in bed and decrease with treatment. We presented a case study in which diagnosed with mitral valve regurgitation, pulmonary embolism and pregnant for 1.5 months. Initial BNP levels of 633 pg/ml decreased to 233, 65.2, 58.4 levels respectively which was parallel to improvements in the clinical state and right ventricle function detected in echocardiography. We used a rapid bedside test for determination of BNP.
Although the evidence that right ventricular (RV) function has significant impact on cardiac hemodynamics and outcome is indisputable, its evaluation has been hampered by problems with image quality, geometric variability, and the absence of a standard of reference. A resurgence of research activity has sought to discern the pathophysiology of RV dysfunction and to explore new methods for measuring performance. Noninvasive techniques such as tissue Doppler echocardiography, three-dimensional echocardiography, and magnetic resonance imaging provide new quantitative information and may improve prediction of outcomes. These advances in technology, and the recognition that RV systolic function is essential in many conditions, provide the impetus for future studies. This review highlights the past and present efforts to incorporate RV systolic function into the mainstream of cardiology practice.
This study was planned to assess whether tissue Doppler imaging is a useful method for the detection of the right ventricular myocardial infarction. Forty-eight patients with acute inferior myocardial infarction and 24 age- and sex-matched healthy controls were included in this study. Twenty-four patients had electrocardiographic signs of inferior myocardial infarction without right ventricular infarction (group I), and the other 24 patients had electrocardiographic signs of inferior myocardial infarction with right ventricular infarction (group II). From the echocardiographic apical four-chamber view, peak systolic, early diastolic, and late diastolic velocities of the tricuspid annulus at the right ventricular free wall were recorded with the use of pulsed-wave Doppler tissue imaging. The tricuspid annular peak tissue Doppler imaging systolic velocity was significantly lower in group I (14.03 +/- 2.57 cm/s, P << 0.005) and in group II (8.50 +/- 0.84 cm/s, P << 0.005) than in controls (16.63 +/- 2.31 cm/s). The tricuspid annular peak systolic (8.50 +/- 0.84 cm/s vs 16.63 +/- 2.31 cm/s) and peak early diastolic (10.99 +/- 3.28 cm/s vs 19.39 +/- 4.3 cm/s) velocities were significantly lower in group II than in group I, as compared with controls ( P << 0.001). Peak early diastolic velocity of tricuspid annulus (10.99 +/- 3.28 cm/s vs 19.39 +/- 4.3 cm/s) was significantly lower in group I than in controls ( P << 0.001); however, late diastolic velocity was significantly lower in group II (15.98 +/- 5.08 cm/s, P << 0.05) than in group I (18.21 +/- 2.63 cm/s, P << 0.05) and in controls (19.02 +/- 5.29 cm/s). The results of this study indicate that tricuspid annular peak systolic and early diastolic velocities are reduced in patients with right ventricular infarction. The velocity of the tricuspid annulus by tissue Doppler imaging is simple and can be used to distinguish whether patients with inferior myocardial infarction have right ventricular infarction.
BACKGROUND: The limitations of exercise electrocardiography in the detection of coronary artery disease includes low sensitivity, especially in isolated right coronary artery (RCA) disease. Recent studies postulated the addition of right precordial leads to the standard exercise ECG (ExT) recording for better detection of right ventricular ischemia. PURPOSE: We tested the hypothesis that the replacement of the standard first precordial lead (V1) with a fourth right chest lead (V4R) can improve the diagnostic accuracy of ExT. MATERIALS AND METHODS: We studied 100 patients (78 men and 22 women, aged 55 +/- 9 years (31-71)) who underwent treadmill ExT (Bruce protocol) and coronary angiography. 52 patients had the V4R lead (Group V4R) instead of V1. The control group (Group V1) included 48 patients with the standard 12-lead ECG. Hemodynamically significant lesions were defined as stenosis > = 50% in left main coronary artery or > = 70% in other arteries. RESULTS: 76 out of 100 patients had significant coronary lesions on the arteriogram, 81% in Group V4R and 71% in Group V1. Overall sensitivity (71% Group V4R vs 79% Group V1), specificity (40% Group V4R vs 21% Group V1) and accuracy (65% Group V4R vs 63% Group V1) of ExT for detection of significant coronary artery disease was similar in both groups. There was also no statistically significant difference in the ability to define an inferior or right ventricle vs. anterolateral ischemia between both groups. Only 5 out of 32 (16%) patients with significant lesions in RCA revealed ST changes in V4R. CONCLUSIONS: In our study, the application of V4R instead of V1 did not significantly change the accuracy of ExT. Typical ECG signs of ischemia in V4R have high specificity, but low sensitivity for RCA disease. Thus, modification of the standard 12-lead scheme cannot be advocated for routine ExT, however although the use of a wider electrocardiographic window (e.g. V3R-V5R) might be more successful for recording right ventricular ischemia.
We encountered a 66-yr-old man with acute left inferior and right ventricular infarction. Tomographic radionuclide ventriculography and Fourier analysis clearly demonstrated reduced wall motion in the inferior walls of both ventricles and markedly delayed phase angles in the inferior right ventricular segment, indicating dyskinesis, which was confirmed by two-dimensional echocardiography and contrast right ventriculography. Four years later, right ventricular dyskinesis was still present and corresponded to a right ventricular perfusion defect on 99mTc-labeled tetrofosmin tomogram. Right ventricular imaging with tomographic radionuclide ventriculography with Fourier analysis and 99mTc-labeled myocardial tomography demonstrates that, even after improved global function and hemodynamics, right ventricular dyskinesis related to right ventricular perfusion defect can be sustained for several years. Thus, these imaging techniques may contribute to diagnosing right ventricular infarction and investigating the pathophysiology.
About half of the patients with symptoms of inferior acute myocardial infarction (MI) of the left ventricle (LV) are found to have proximal occlusion of the dominant right coronary artery presented on ECG by ischemia or infarction of the right ventricular wall. Hypotension, high pressure in the jugular veins and, in some cases, shock with clear lung fields--typical clinical picture of right ventricular MI. The diagnosis begins with ECG picture of LV lower wall ischemia (rise of ST wave in leads II, III and aVF) with possible emergence of a pathological wave Q and right ventricular ischemia (rise of ST wave in leads V3R-V6R and its depression in leads V2-V4). Echo-CG and balanced radioventriculography were used for verification of the diagnosis, precise localization of the myocardial lesion. Therapy of patients with right ventricular MI consists in maintenance of adequite preload of the right ventricle, inotropic support and control over atrioventricular conduction.
OBJECTIVE: To investigate the effect of obstructive sleep apnea syndrome(OSAS) on the right cardiac structure and function. METHODS: The right cardiac structure and function were measured by using M-mode and two-dimension echocardiography in 30 OSAS patients. RESULTS: In moderate and severe OSAS groups, the right ventricular end diastolic volume (RVEDV), stroke volume (SV) and right pulmonary artery inner diameter (RPAD) increased markedly, and the E/A of the right ventricular decreased in the meantime as compared with the control group. CONCLUSION: OSAS not only effects the right cardiac structure, but also the right cardiac systolic and diastolic function.
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Acute right heart failure in a young person is an unusual presentation and drug overdose is a rare cause. A case is described where the patient presented with striking clinical signs of acute pulmonary hypertension and right heart failure, which were confirmed by transthoracic echocardiography. The precipitating event appeared to be poisoning by tramadol. There were features in keeping with tramadol toxicity and serotonin syndrome. The possible pathophysiology behind the process is discussed.
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