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Postinfarction ventricular septal rupture: the importance of location of infarction and right ventricular function in determining survival.

Over a 5.5 year period, 1264 consecutive patients with acute myocardial infarction as confirmed by enzyme levels were prospectively identified. Of these, 25 (2%) suffered ventricular septal rupture (pulmonary/systemic flow range 1.5 to 6) 7 +/- 7 days after onset of myocardial infarction. Death occurred in 14 patients (56%) and was more common after inferior than anterior myocardial infarction (11 of 15 [73%] vs three of 10 [30%], p less than .05). Among 133 variables analyzed, survivors and nonsurvivors were similar with respect to all premorbid clinical characteristics, infarct size as assessed by peak creatine kinase values, shunt size, two-dimensional echocardiographic and hemodynamic indexes of left ventricular function, and extent of coronary disease. Compared with survivors, the nonsurvivors had greater impairment of right ventricular function as determined by a higher two-dimensional echocardiographically derived right ventricular wall motion index (RVWMI) (0.55 +/- 0.87 vs 1.70 +/- 0.45, p less than .001), greater elevation of right ventricular end-diastolic pressure (11 +/- 6 vs 17 +/- 6, p less than .02), and greater mean right atrial pressure (10 +/- 6 vs 16 +/- 3, p less than .01). Of interest, two of the three patients who presented with anterior myocardial infarction and who died had inferiorly extended infarcts and all had abnormal RVWMIs (greater than or equal to 1.0). As expected, cardiogenic shock shortly after onset of ventricular septal rupture was associated with a 91% mortality, but was more common after inferior than anterior myocardial infarction (60% vs 20%, p less than .05). The mean effective cardiac index was also higher in survivors than nonsurvivors (2.1 +/- 0.5 vs 1.2 +/- 0.5, p less than .001). Finally, multivariate analysis indicated that all nonsurvivors could be identified based on: an effective cardiac index of 1.75 liters/min/m2 or less, the presence of extensive right ventricular and septal dysfunction on the two-dimensional echocardiogram, a mean right atrial pressure of 12 mm Hg or more, and early onset of ventricular septal rupture. Thus, our data demonstrate that: mortality is higher when ventricular septal rupture complicates inferior than when it complicates anterior myocardial infarction, survivors can be distinguished from nonsurvivors and the prediction of outcome is highly accurate, and combined right ventricular and septal dysfunction has a substantial impact on prognosis.

Adult↗

Right heart dysfunction in post-tuberculosis emphysema.

SETTING: University-affiliated general hospital. OBJECTIVE: To evaluate the pump performance of right heart before and after exercise in post-tuberculosis emphysema. DESIGN: In patients with post-tuberculosis or primary emphysema (similar lung volumes), body plethysmography, arterial blood gas analysis and echocardiography were performed at rest and after exercise. Right heart pump performance was evaluated with the ejection fraction. RESULTS: At rest, in post-tuberculosis emphysema, diffusing capacity (mean +/- SE 72.7 +/- 3.9 vs. 91.0 +/- 7.1% of reference) and right ventricular ejection fraction (57.5 + 1.4 vs. 61.3 +/- 1.2%) were lower and PaCO2 (42.7 +/- 1.1 vs. 38.6 +/- 0.7 mmHg) was higher, while lung compliance, airway resistance, PaO2, and alveolar-arterial oxygen difference were not different. After exercise, PaO2 (65.6 +/- 2.8 vs. 80.5 +/- 3.5 mmHg) and right ventricular ejection fraction (51.2 +/- 2.4 vs. 59.6 +/- 1.7%) were lower and PaCO2 (47.0 +/- 1.5 vs. 40.9 +/- 1.5 mmHg) was higher in post-tuberculosis emphysema, whereas alveolar-arterial oxygen difference was not different. PaCO2 and alveolar-arterial oxygen difference increased, and PaO2 and right ventricular ejection fraction decreased in post-tuberculosis emphysema, while they did not significantly change in primary emphysema. CONCLUSION: In post-tuberculosis emphysema, the impairment of gas exchange was more serious. Global assessment should be focused on right heart dysfunction which might be more affected than in primary emphysema.

Blood Gas Analysis↗

[Significance of 123I-metaiodobenzylguanidine SPECT for detecting left ventricular involvement in patients with arrhythmogenic right ventricular dysplasia].

The right ventricle being primarily involved in ARVD, recent reports indicate the presence of histological and functional abnormalities in the left ventricle for some patients with ARVD. The aim of this study was to evaluate the significance of myocardial sympathetic dysfunction as an early sign of left ventricular (LV) involvement by 123I-MIBG (MIBG) SPECT and to compare the findings with those of 201TlCl (Tl) SPECT, radionuclide left ventriculography, ultrafast computed tomography (UFCT), magnetic resonance imaging (MRI) and echo-cardiography in 10 patients (pts) with ARVD. MIBG defects in LV regions were detected in 9 pts. Seven of the 9 pts showed MIBG defects in LV regions adjacent to RV. The subjects were divided into 2 groups based on left ventriculography, 5 with normal LVEF (> 55%) and 5 with reduced LVEF. In the normal LVEF group, 4 pts showed MIBG defects and 2 pts showed TI defects, and MIBG defects were larger than TI defects (ES: 14 +/- 6 vs. 5 +/- 7, p <0.05). In reduced LVEF group, all of 5 pts showed MIBG and TI defects, and MIBG defects were larger than TI defects (ES: 42 +/- 12 vs. 25 +/- 3, p <0.05). In comparison with normal LVEF group, reduced LVEF group showed larger and more severe MIBG defects (ES: 42 +/- 12 vs. 14 +/- 6, p <0.01, SS: 44 +/- 31 vs. 8 +/- 7, p <0.05). UFCT and MRI showed abnormal findings indicating LV fatty infiltration in only 3 of reduced LVEF group. Thus, MIBG showed abnormal distributions in the left ventricle with the highest frequency in all these modalities. These results suggest that MIBG SPECT provides a sensitive marker for detecting LV involvement in ARVD. Also, the extent of MIBG distribution abnormalities is helpful in assessing the severity of left ventricular involvement in patients with ARVD.

3-Iodobenzylguanidine↗

[Effects of perstarium on the systolic and diastolic functions of the myocardium in patients with chronic cardiac failure].

The aim of the study was to assess prestarium effects on systolic and diastolic cardiac functions in 38 patients with ischemic heart disease and chronic cardiac failure (NYHA functional class II-IV) by biventricular balanced radioventriculography. Both left and right ventricular diastolic dysfunction was found. A course of prestarium treatment caused different alterations in ventricular contractility. 64.2% patients of those who had right ventricular ejection fraction < 40% achieved an increase in right and left ventricular ejection fraction. Improved diastolic function of the myocardium was registered in 71% patients.

Adult↗

Atrialization of right ventricular pressure during acute cardiac allograft rejection.

We describe a patient who, during an episode of acute cardiac rejection, developed such severe systolic dysfunction that there was transient near-adynamic function of the right ventricle. This right ventricular dysfunction was reflected hemodynamically by the unusual finding of atrialization of right ventricular pressures. The patient's cardiac function returned to normal after treatment with extensive immunotherapy.

Acute Disease↗

Arrhythmogenic right ventricular dysplasia presenting as right ventricular outflow tract tachycardia.

A case of a 51-year old male is presented. A left bundle branch block inferior axis tachycardia was manifest. At electrophysiological study this tachycardia was inducible and was ablated in the septal right ventricular outflow tract (RVOT). Two other tachycardias were identified both with right bundle branch block (RBBB) morphology raising the suspicion of diffuse pathology. Arrythmogenic right ventricular dysplasia (ARVD) was confirmed by right ventricular angiography and magnetic resonance imaging (MRI). An implantable cardioverter defibrillator (ICD) was implanted and an appropriate shock was later delivered.

Arrhythmogenic Right Ventricular Dysplasia↗

Symptoms and management options in cardiomyopathy.

Cardiomyopathy is the most common cause of sudden cardiac death in young people, including trained athletes (Maron et al, 1996). Often the tragedy of sudden death is the first indication of its presence within a family. This article describes the four types of cardiomyopathy, diagnosis, treatment and management options, and discusses ways in which the new National Service Framework for Coronary Heart Disease (Department of Health, 2005) will help in planning and implementing services.

Arrhythmogenic Right Ventricular Dysplasia↗

Generation of reactive O2 species in the myocardium of newborn lambs following intrauterine increase in right ventricular pressure.

Fetuses with pulmonary stenosis and constriction of the ductus arteriosus or the recipient twin in the context of a twin-to-twin transfusion syndrome may present with severe right ventricular myocardial dysfunction. Free O2 radicals are known to be increased in hypertrophied adult myocardium secondary to an increase in endocavitary pressure. This study investigates whether products of reactive O2 species generation are abnormally elevated in the myocardium of fetuses with increased right ventricular pressure. Banding of the main pulmonary artery was performed in five fetal lambs at 90 to 100 days of gestation. Three other animals had a sham intervention and were used as controls. Postoperative observation lasted on average 42 days (range 33-49 days). The levels of hydroperoxides were found to be significantly higher in the right ventricle of the stenosed lambs (6.6 +/- 3.5 nmol/mg protein) compared to the left ventricle of the same lambs (0.7 +/- 0.7 nmol/mg protein), and compared to the right (0.12 +/- 0.1 nmol/mg protein) and the left (0.5 +/- 0.8 nmol/mg protein) ventricles of the controls. It is concluded that during fetal life, an increase in right ventricular pressure is associated with a marked accumulation of products of reactive O2 species generation in the right ventricular myocardium.

Animals↗