Regional right ventricular dysfunction in acute pulmonary embolism and right ventricular infarction.

BACKGROUND: A normally contracting right ventricular apex associated to a severe hypokinesia of the mid-free wall ('McConnell sign') has been considered a distinct echocardiographic pattern of acute pulmonary embolism. OBJECTIVE: To evaluate the clinical utility of the 'McConnell sign' in the bedside diagnostic work-up of patients presenting to the Emergency Department with an acute right ventricular dysfunction due to pulmonary embolism or right ventricular infarction. DESIGN: Among 201 patients, consecutively selected from our clinical database and diagnosed as having massive or submassive pulmonary embolism or right ventricular infarction, 161 were suitable for an echocardiographic review of regional right ventricular contraction and were included in the study. There were 107 cases with pulmonary embolism (group 1) and 54 cases with right ventricular infarction (group 2). All echocardiographic studies were randomly examined by two experienced and independent echocardiographers, blinded to the patient diagnosis and without Doppler informations. RESULTS: The McConnell sign was detected in 75 of 107 patients in group 1 (70%) and in 36 of 54 patients in group 2 (67%); the finding was absent in 32 cases in group 1 and in 18 cases in group 2 (P=0.657). The sensitivity, specificity, positive and negative predictive values of the McConnell sign for the diagnosis of pulmonary embolism were respectively 70, 33, 67 and 36%. CONCLUSIONS: In a clinical setting of patients with acute right ventricular dysfunction the McConnell sign cannot be considered a specific marker of pulmonary embolism.     

Acute right ventricular infarction secondary to massive pulmonary embolism

Isolated right ventricular infarction has been found in casesof right ventricular hypertrophy, but there are no reports onright ventricular infarction secondary to massive pulmonaryembolism. Six autopsied patients with massive pulmonary embolismand pure right ventricular infarction, suspected to be secondaryto the embolism, were selected from a population of 216 autopsies.Pulmonary embolism was the suspected diagnosis in five casesdue to typical clinical, electrocardiographic and haemodynamicdata. Right ventricular infarction was a post-mortem finding,not previously diagnosed. In every case the thickness of theright ventricular myocardium was normal. The necrosis of theright ventricle was transmural in four cases and subendcardialin two and the entire right ventricular wall (anterolateralas well as posterior) was involved. No mural thrombi were presentand in no case did the necrosis involve the left ventricle.In one case the coronary arteries were normal, in the otherfive significant lesions of the right or the left coronary arterieswere observed. These lesions may have been, in part, responsiblefor the necrosis of the right ventricle when the massive pulmonaryembolism was added. We conclude that right ventricular infarctionmay be secondary to pulmonary hypertension in the setting ofmassive pulmonary embolism, even in the absence of right ventricularhypertrophy and with normal or stenotic coronary arteries.     

Pulmonary embolism with isolated right ventricular infarction.

Concomitant occurrence of pulmonary embolism and right ventricular infarction is rare. It poses important diagnostic and therapeutic implications. A case of pulmonary embolism with isolated right ventricular anterior wall infarction presented with ventricular tachycardia. One pathology could have led to the other. Two-dimensional echocardiography was useful in documenting pulmonary artery hypertension as well as regional wall motion abnormality of the right ventricle. Thrombolytic therapy and dobutamine infusion were useful. Nitrates, fluid infusion and diuretics should be used cautiously.     

Isolated right ventricular aneurysm following right ventricular infarction

A 78-year-old man with atherosclerotic heart disease developed extensive right ventricular infarction fibrosis with aneurysm formation following right coronary artery occlusion. No symptoms of right-sided heart failure were present. Postmortem examination revealed that 40% of the right ventricle, 11% of the septum and 7% of the left ventricular free wall were infarcted due to right coronary artery occlusion. This is the first documented case of isolated aneurysm of the right ventricle following infarction and it demonstrates that even extensive right ventricular destruction may be present without symptoms.     

Cardiac inflammation contributes to right ventricular dysfunction following experimental pulmonary embolism in rats

Acute right ventricular (RV) failure following pulmonary embolism (PE) is a strong predictor of poor clinical outcome. Present studies test for an association between RV failure from experimental PE, inflammation, and upregulated chemokine expression. Additional experiments test if neutrophil influx contributes to RV dysfunction. PE was induced in male rats by infusing 24 microm microspheres (right jugular vein) producing mild hypertension (1.3 million beads/100 g, PE1.3), or moderately severe hypertension (2.0 million beads/100 g, PE2.0). Additional rats served as vehicle sham (0.01% Tween 20, Veh). In vivo RV peak systolic pressures (RVPSP) increased significantly, and then declined following PE2.0 (51 +/- 1 mm Hg 2 h; 49 +/- 1, 6 h; 44 +/- 1, 18 h). RV generated pressure of isolated, perfused hearts was significantly reduced in PE2.0 compared with PE1.3 or Veh. MCP-1 protein (ELISA) was elevated 21-fold and myeloperoxidase activity 95-fold in RV of PE2.0 compared with Veh or PE1.3. CINC-1, CINC-2, MIP-2, MCP-1, and MIP-1alpha mRNA also increased in RV of PE2.0. Histological analysis revealed massive accumulation of neutrophils (selective esterase stain) and monocyte/macrophages (CD68, ED-1) in RV of PE2.0 hearts in regions of myocyte damage. Electron microscopy showed myocyte necrosis and phagocytosis by inflammatory cells. LV function was normal and did not show increased inflammation after PE2.0. Treatment with anti-PMN antibody reduced RV MPO activity and prevented RV dysfunction. Conclusions-PE with moderately severe pulmonary hypertension (PE2.0) resulted in selective RV dysfunction, which was associated with increased chemokine expression, and infiltration of both neutrophils and monocyte/macrophages, indicating that a robust immune response occurred with RV damage following experimental PE. Experimental agranulocytosis reduced RV, suggesting that neutrophil influx contributed to RV damage.     

Isolated right ventricular noncompaction caused ventricular tachycardia and pulmonary embolism

Isolated ventricular noncompaction is an unclassified cardiomyopathy due to intrauterine arrest of compaction of the loose interwoven meshwork. Its mortality and morbidity are high, including heart failure, thromboembolic events, and ventricular arrhythmias. Isolated right ventricular noncompaction was reported rarely, especially that causes pulmonary embolism and ventricular tachycardia. We describe a case of isolated noncompaction of the right ventricular causing pulmonary embolism and ventricular tachycardia.     

Massive pulmonary embolism associated with a right ventricular myxoma

A 12 year old boy had a massive pulmonary embolism associated with a right ventricular myxoma. This caused complete occlusion of the main trunk of the left pulmonary artery and of a branch of the right pulmonary artery supplying the basal area of the lower lobe of the right lung. The patient died despite two surgical attempts to remove the tumor clots. To our knowledge this constitutes the first report of a massive pulmonary artery embolism associated with a right ventricular myxoma.     

Pure right ventricular infarction.

A 76-year-old man with chest pain was admitted to hospital where electrocardiography (ECG) showed ST-segment elevation in leads V1-4, indicative of acute anterior myocardial infarction. ST-segment elevation was also present in the right precordial leads V4R-6R. Emergency coronary angiography revealed that the left coronary artery was dominant and did not have significant stenosis. Aortography showed ostial occlusion of the right coronary artery (RCA). Left ventriculography showed normal function and right ventriculography showed a dilated right ventricle and severe hypokinesis of the right ventricular free wall. Conservative treatment was selected because the patient's symptoms soon ameliorated and his hemodynamics was stable. 99mTc-pyrophosphate and 201Tl dual single-photon emission computed tomography showed uptake of 99mTc-pyrophosphate in only the right ventricular free wall, but no uptake of 99mTc-pyrophosphate and no perfusion defect of 201Tl in the left ventricle. The peak creatine kinase (CK) and CK-MB were 1,381 IU/L and 127 IU/L, respectively. His natural course was favorable and the chest pain disappeared under medication. Two months after the onset, the ECG showed poor R progression in leads V1-4 indicating an old anterior infarction. Coronary angiography confirmed the ostial stenosis of the hypoplastic RCA. This was a case of pure right ventricular free wall infarction because of the occlusion of the ostium of the hypoplastic RCA, but not of the right ventricular branch. Because the electrocardiographic findings resemble those of an acute anterior infarction, it is important to consider pure right ventricular infarction in the differential diagnosis.     

Isolated right ventricular infarction.

The literature on isolated right ventricular infarction is reviewed and local experience is reported. Chronic lung disease is an important risk factor. Chest pain and breathlessness are common. Syncope and sudden collapse can also occur. Rhythm disorders include sinus bradycardia, atrial fibrillation and ventricular tachycardia or fibrillation. Atrioventricular block is rare. Hypotension and a right-sided fourth heart sound are common. Cautious use of slow-release nitroglycerin is not hazardous in the absence of hypotension. High doses of steroids and anticoagulants can be helpful. The prognosis is usually good, although sudden collapse can occur due to ventricular fibrillation, rupture of the right ventricular free wall or massive pulmonary embolism.     

Disturbance of pulmonary gas exchange in patients with right ventricular infarction.

To evaluate the difference in pulmonary gas exchange in patients with and without right ventricular infarction, 147 consecutive patients with their first inferior wall Q-wave acute myocardial infarction were studied. Thirty-nine patients (group 1) had electrocardiographic evidence of right ventricular infarction and it was absent in 108 patients (group 2). A significantly wider alveolar arterial oxygen difference and higher roentgenographic scores were observed in group 1 compared with group 2. Although there were no significant differences in pulmonary artery wedge pressure and colloid osmotic pressure between groups 1 and 2, mean right atrial pressure was significantly higher, while cardiac output and mixed venous oxygen saturation were lower in group 1 compared with group 2. Patients in group 1 had significantly more left ventricular segments with advanced asynergy and higher incidence of proximal right coronary artery lesions than those in group 2. Thus, our data suggest that disorder of pulmonary gas exchange in patients with right ventricular infarction may be explained by increased permeability of the alveolar capillary membrane secondary to larger extent of ischemic myocardium and by hemodynamic abnormalities associated with right ventricular infarction.     

Thrombolysis of mobile right atrial thrombi following severe pulmonary embolism

Thrombolysis may favorably affect the clinical outcome of mobile right atrial thrombus following pulmonary embolism (PE). We report the case of three patients with mobile right atrial thrombus following PE, in whom fibrinolysis was performed. Atrial mass disappeared on the control echocardiogram, but control ventilation perfusion scan showed new perfusion defects in all patients. Thrombolysis seems successful for the treatment of patients with mobile right atrial thrombus following PE; however, recurrent PE may be induced by fibrinolysis. This may affect the benefit of such therapy and should be taken into account when using this therapeutic treatment.     

Prognostic role of biomarkers and right ventricular dysfunction in pulmonary embolism

Pulmonary embolism is morbidity and mortality remain high. The short-term prognosis of pulmonary embolism depends on haemodynamic status and underlying disease massive pulmonary embolism, defined as pulmonary embolism that is associated with systemic hypotension which increases up to 50% in hospital mortality. However, the in-hospital mortality of patients with normal blood pressure pulmonary embolism has been reported to vary from 3 to 15%. Right ventricular dysfunction showed by echocardiography or computerized tomography and elevated cardiac enzymes have been used to determine mortality in these patients with pulmonary embolism. In this article; we reviewed the prognostic value of right ventricular dysfunction as evaluated by echocardiography or spiral computerized tomography, and the prognostic value of increased levels of cardiac markers in patients with pulmonary embolism.     

Recovery of regional right ventricular function after thrombolysis for pulmonary embolism

Abnormalities in right ventricular regional and global function can occur in the setting of acute pulmonary embolism. Treatment of acute pulmonary embolism with thrombolysis is associated with significant improvement in regional and global right ventricular function.