Collateral vessel development after right ventricular infarction in the pig

Although the right coronary artery supplies both ventricles in the pig, a gradual proximal right coronary occlusion produces infarction in the left ventricle, whereas the right ventricle is usually spared. This study evaluates the influence of right ventricular hypertension and hypertrophy (RVHH) on the occurrence of right ventricular infarction and the difference in the rate and extent of collateral vessel development after gradual right coronary occlusion in pigs with (RVHH group) and without (control group) increased right ventricular pressure and mass. Right ventricular hypertension and hypertrophy were induced by pulmonary arterial banding which raised right ventricular systolic pressure from 24 to 74 mm Hg and doubled right ventricular mass in 4 weeks. Right coronary occlusion was produced with an ameroid constrictor in 24 control group pigs and 15 RVHH pigs. Serial selective coronary cineangiograms on days 4, 8, 14, 21 and 28 after ameroid constrictor placement showed no difference in first appearance of collateralization to the occluded right coronary artery. Total collateralization, which was present in all pigs studied in the control group by days 21 and 28, was present in only 57 percent of the RVHH group at the same time. Although left ventricular infarction occurred in all animals in both groups, right ventricular infarction was not found in the control group but was seen in 80 percent of the RVHH group. There was no correlation between the degree of collateralization seen and the size of the right ventricular infarction found. Experimentally induced right ventricular hypertrophy and hypertension make the right ventricle susceptible to infarction and impeded total collateral filling of the occluded right coronary artery in some of the animals studied.     

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.     

Right ventricular infarction with tricuspid insufficiency and chronic right heart failure.

A patient with chronic right heart failure and probable tricuspid insufficiency associated with an inferior myocardial infartion is described. Angiograms demonstrated total occlusion of the right coronary artery at its origin, a patent venous bypass graft to the mid-right coronary artery and hypokinesia of the inferior wall of both the right and left vebtricles. Clinical data indicated a greater impairment of right than of left ventricular function. It is proposed that infarction of the right ventricle resulted in chronic right heart failure and tricuspid insufficiency.     

Acute right ventricular infarction without infero-posterior left ventricular infarction

Two cases of acute right ventricular infarction associated with acute extensive anterior myocardial infarction in the absence of inferior and/or posterior left ventricular infarction are presented. Such a combination is likely to occur from acute occlusion of the left anterior descending artery in the face of severe narrowing of the infundibular (conus) artery rather than from acute occlusion of the right coronary artery.     

Isolated right ventricular infarction due to occlusion of the right ventricular branch in the absence of percutaneous coronary intervention

Isolated right ventricular myocardial infarction accounts for only 3% of all infarctions. It has previously been reported as a complication of percutaneous coronary intervention involving the right coronary artery secondary to occlusion of the right ventricular branch. In the present report, a patient is described in whom isolated right ventricular myocardial infarction developed due to occlusion of the right ventricular branch of the right coronary artery in the absence of percutaneous intervention.     

Isolated right ventricular infarction resulting from thrombotic occlusion of a hypoplastic right coronary artery

Three cases of isolated right ventricular infarction resulting from thrombotic occlusion of a hypoplastic right coronary artery were found in 4,000 consecutive autopsies performed at Tokyo Metropolitan Geriatric Hospital. The incidence of isolated right ventricular infarction was 0.08%. The clinical profile of the first case was characterized by shock, pulmonary congestion, pleural effusion, decreased V1R and V2R on ECG, a small elevation of CPK and transaminase, elevation of fibrin degenerative products and decreased platelet count. The patient responded to volume expansion, heparin and catecholamines. One year later she died from cerebral bleeding. In the second case, mild aortic regurgitation and atrial fibrillation were present. He died suddenly during an episode of pneumonia. In the third case, there was chronic obstructive lung disease, atrial fibrillation and lung cancer. He died of respiratory failure. On autopsy, the coronary arteries revealed a marked left dominant and right hypoplastic pattern in all cases. The right coronary artery perfused only the free wall of the right ventricle. Complete occlusion of the hypoplastic right coronary artery resulted in isolated right ventricular infarction. In addition, chronic pulmonary disease and arrhythmia may be contributory.     

Anterior ST-segment elevation with right coronary artery occlusion: a unique case of isolated right ventricular infarction

Anterior ST-segment elevation is the classic electrocardiographic feature of anterior left ventricular myocardial infarction due to occlusion of the left anterior descending artery. However, anterior ST-segment elevation has also been described in patients with right coronary artery occlusion, in whom concomitant inferior ST-segment elevation is also typically present. A case of proximal right coronary artery occlusion resulting in anterior ST-segment elevation without inferior ST-segment elevation is reported in this article. It is hypothesized that the inferior left ventricular wall was protected by left-to-right collaterals, as seen on coronary angiography, with resultant isolated right ventricular infarction upon proximal right coronary artery occlusion. In conclusion, this report presents a unique case of an isolated right ventricular infarction resulting in an electrocardiographic pattern mimicking anterior-wall left ventricular infarction.     

Left ventricular pump function in right ventricular overload

To clarify how left ventricular pumping action is altered in cor pulmonale, an experimental study was performed using canine heart preparations in which the effects on left ventricular performance of right ventricular overload, with and without depressed systolic function, were investigated. For this purpose, two methods using excised perfused hearts (n = 16) and in vivo hearts (n = 6) were employed, and in the latter condition, pulmonary artery constriction (n = 7), femoral arterial-venous (A-V) shunt (n = 3) and right coronary artery occlusion (n = 6) were induced. Left ventricular systolic function was assessed by the relationship between left ventricular isovolumic developed pressure and left ventricular volume in excised heart, and by ejection fraction with 2 dimensional echocardiogram in the vivo condition, taking into account preload and afterload changes. From the excised heart preparation, it was shown that left ventricular developed pressure significantly decreases when right and left ventricular diastolic pressure increases greatly. On the other hand, in vivo right ventricular overload due to pulmonary constriction and A-V shunt, the left ventricular ejection fraction increased following afterload reduction. When we compare the left ventricular ejection fraction in pulmonary constriction with that in right coronary occlusion, in which reduction of left ventricular diastolic area from the control was similar, the latter was significantly decreased despite afterload reduction. These results suggest that right ventricular overload does not necessarily induce left ventricular systolic dysfunction unless left ventricular end-diastolic pressure, as well as that of the right ventricle, increases definitely and simultaneously.(ABSTRACT TRUNCATED AT 250 WORDS)     

Nondominant right coronary artery occlusion presenting with isolated right ventricular infarction and ventricular fibrillation

It is generally believed that serious complications are unlikely in a myocardial infarction resulting from occlusion of a nondominant right coronary artery. A case of isolated right ventricular infarction caused by total occlusion of a nondominant right coronary artery complicated by two episodes of ventricular fibrillation is presented.     

Right ventricular infarction: frequency, size and topography in coronary heart disease: a prospective study comprising 107 consecutive autopsies from a coronary care unit

During a 14 month period autopsies were performed on 107 patients with coronary heart disease and the results were evaluated prospectively with special reference to right ventricular infarction. A total of 214 regional infarcts were found, 107 (50%) of which involved the right ventricle. Right ventricular infarction was found in 90 hearts (84%), but only three isolated right ventricular infarcts were seen. Right ventricular involvement was found with equal frequency in anterior and posterior infarction (64 versus 66%), but posterior right ventricular infarcts were much larger (15% of the right ventricle was infarcted versus 1%). Proximal right coronary artery occlusion caused larger right ventricular infarction than did distal occlusion (15 versus 5 g). Right ventricular infarct size was not influenced by coronary artery disease (evaluated angiographically) in noninfarct-related vessels. Anterior right ventricular infarcts were predominantly located near the apex of the heart (to the left of the sternum), whereas posterior right ventricular infarcts were located near the atrioventricular groove (along the right sternal border). Infarct size was equal in patients who died from a first acute anterior or posterior infarct. However, posterior infarcts had more right ventricular involvement (28% of total infarct size versus 7% in anterior infarcts) leaving more of the left ventricular myocardium intact (79 versus 64%). These differences in infarct topography may explain why right ventricular involvement seldom is diagnosed clinically in patients with anterior infarction, and why left ventricular function and prognosis usually are better after posterior compared with anterior infarcts of enzymatically equal size.     

Large ventricular aneurysms occurring after myocardial infarction

We have studied 33 patients with a large ventricular aneurysm complicating an anterior myocardial infarction. The features of myocardial infarction progressing towards an aneurysm were no previous history of coronary disease, severe infarction as shown by the severity of pain and the presence of pericardial rub and heart failure, and large increase in serum levels of cardiac enzymes. A large aneurysm usually follows a large infarction resulting from the total or partial occlusion of the left anterior descending artery, which is involved alone in about half the patients and is associated with lesions of the circumflex and right coronary arteries in the other half. In most cases, standard radiography showed an abnormal cardiac configuration, but in 7 patients (21%) there was no radiological evidence of aneurysm. ST segment elevation (mean 2.7 mm) was reported in all subjects but one. Heart failure was present in most patients and was an indication for surgical treatment in one-third of the patients. A large aneurysm was not a contraindication to operation even when at angiography the aneurysm seemed to occupy almost all the left ventricle. Twenty-one patients were operated upon for resection of the aneurysm with a mortality rate of 14 per cent.     

Large ventricular aneurysms occurring after myocardial infarction.

We have studied 33 patients with a large ventricular aneurysm complicating an anterior myocardial infarction. The features of myocardial infarction progressing towards an aneurysm were no previous history of coronary disease, severe infarction as shown by the severity of pain and the presence of pericardial rub and heart failure, and large increase in serum levels of cardiac enzymes. A large aneurysm usually follows a large infarction resulting from the total or partial occlusion of the left anterior descending artery, which is involved alone in about half the patients and is associated with lesions of the circumflex and right coronary arteries in the other half. In most cases, standard radiography showed an abnormal cardiac configuration, but in 7 patients (21%) there was no radiological evidence of aneurysm. ST segment elevation (mean 2.7 mm) was reported in all subjects but one. Heart failure was present in most patients and was an indication for surgical treatment in one-third of the patients. A large aneurysm was not a contraindication to operation even when at angiography the aneurysm seemed to occupy almost all the left ventricle. Twenty-one patients were operated upon for resection of the aneurysm with a mortality rate of 14 per cent.     

Changes in right ventricular relaxation during acute anterior myocardial infarction in pigs

To determine the effect of an anteroseptal myocardial infarction on right ventricular systolic and diastolic function, we studied 12 pigs before and 1 h after left anterior descending coronary artery occlusion. Total arterial occlusion was achieved by the percutaneous, transcatheter placement of a 1 mm Teflon plug into the mid portion of the artery. The resulting infarction involved 28 (SEM 3)% of the left ventricular wall, in the anterior and septal regions. A small rim of the right ventricular free wall adjacent to the septum and the right ventricular apex were also affected. End diastolic pressures in both ventricles rose significantly: left ventricular from 12(1) to 20(2) mm Hg and right ventricular from 8(1) to 10(1) mm Hg. Right ventricular peak systolic pressure increased from 29(2) to 35(2) mm Hg while left ventricular peak systolic pressure did not change. One hour after infarction the half time of isovolumic relaxation of the right ventricle was prolonged from 6.9(0.5) to 8.7(0.4) ms. Ejection fraction in both ventricles was depressed: from 46(1) to 34(2)% in the right ventricle and from 69(3) to 49(3) in the left ventricle. There was no change in either right or left ventricular dP/dt. These data suggest that right ventricular systolic and diastolic dysfunction occurs as the result of an anteroseptal myocardial infarction in pigs.     

Clinical characteristics of postinfarction left ventricular aneurysm with extensive calcification]

The authors experienced 4 cases of calcified postinfarction aneurysm of the left ventricle. They were all male, aged 55 to 71 (mean 64). Risk factor for coronary artery disease was only smoking in 2 patients, but there was none in the others. They had had acute anteroseptal or extensive anterior infarction at age 41-57 years (mean 49.3), and associated major cardiac events 10-22 years (mean 14.5) after acute myocardial infarction. Ventricular tachycardia, congestive heart failure and systemic thromboembolism were seen in 4, 2 and 1 patients respectively. However, none developed angina pectoris. In the 2 patients in whom signal-averaged electrocardiogram was performed, late potential was detected, so it was suspected that ventricular tachycardia could be due to reentry. Left ventricular end-diastolic pressure was elevated in all patients except one and ranged from 11 to 22 mmHg. Left ventricle was dilated in all cases and the end-diastolic volume index ranged from 143 to 503 ml/m2. The left ventricular ejection fraction ranged from 11 to 24%. However, in 2 of the 4 patients, the cardiac index was within normal limits, and evidence of congestive heart failure was absent. In 2 other patients with associated congestive heart failure, cardiac indices were 2.32, 1.56 l/min/m2 respectively. Coronary arteriogram showed a total occlusion in the left anterior descending (LAD) artery in all cases, and only the LAD artery was affected in 2 patients. In the remaining 2 patients, the right coronary arteries also were significantly stenotic or totally occluded, i.e., they had 2-vessel disease.(ABSTRACT TRUNCATED AT 250 WORDS)     

Scintigraphic evidence that the right ventricular myocardium tolerates ischaemia better than the left ventricular myocardium

To study the incidence of right ventricular infarction and theeffect of intracoronary thrombolysis on the ischaemic rightventricular myocardium, we performed intracoronary myocardialthallium scintigraphy in 18 patients with complete occlusionof the right coronary artery who underwent intracoronary thrombolysis.In 15 of these patients, intracoronary thallium-201 and technetium-99m pyrophosphate scintigrams were performed simultaneously. All18 patients had a right ventricular thallium defect before thrombolysis,and all had new thallium uptake after thrombolysis. 17 out of18 patients had a left ventricular thallium defect before thrombolysis,but only 10 of them showed new thallium uptake after thrombolysis.14 out of 15 patients had a left ventricular technetium-99 mpyrophosphate spot after thrombolysis and some diffuse pyrophosphateaccumulation in the area of the right ventricle. In one patientpyrophosphate accumulation was found only in the area of theright ventricle. Thus, right ventricular thallium defects weredetected by intracoronary thallium scintigraphy in the majorityof patients with inferior acute myocardial infarction due toright coronary artery occlusion. Right ventricular thalliumdefects were always reversible in contrast to left ventricularthallium defects in the same patients, suggesting that rightventricular myocardium tolerates ischaemia better than leftventricular myocardium.     

Occlusion of the right coronary artery with acute right heart infarct and cardiogenic shock

In a 42-year-old patient with an acute inferior infarction the right coronary artery was recanalised by intracoronary streptokinase 4 hours after the onset of symptoms. In spite of early reperfusion the patient developed an extensive myocardial infarction and died three days later from cardiogenic shock. Autopsy revealed an almost complete necrosis of the right ventricle including the inferior interventricular septum and the adjacent left ventricular wall. Diagnostic and therapeutic problems in the so-called dominant right ventricular infarction are discussed.     

Divergent time courses of ventricular vulnerability of the heart to ventricular tachycardias and ventricular fibrillation in the early necrosis stage of acute experimental myocardial infarct

Early necrosis in acute experimental myocardial infarction is characterized by severe ventricular dysrhythmias beginning approx. 6 hours after coronary artery occlusion and persisting for 2-5 days. It was the aim of this study to investigate the comparative changes in ventricular vulnerability to spontaneous and stimulus-induced tachycardia and fibrillation during early necrosis 6-18 hours following acute coronary artery occlusion. Results: 1) The thresholds for repetitive extrasystoles and for ventricular fibrillation determined via electrodes placed on to the endocardium of the right and left ventricle outside of the ischemic area are within the normal range of the non-ischemic heart. 2) Both stimulation thresholds increase significantly within the area of infarction and in many cases are not inducible any more after 18 hours of ischemia, whatever amount of current is applied. 3) Sustained ventricular tachycardia can be induced in about 30% of cases after an occlusion lasting approx. 6 hours and in about 80% after an occlusion period of 18 hours. 4) Electrically induced ventricular tachycardias differ from spontaneously occurring VT in so far as the former appear to be due to a reentry mechanism, whereas the latter seem to be "accelerated ventricular rhythms" and thus of focal origin. Our results demonstrate that enhanced ventricular vulnerability during early necrosis in acute myocardial infarction is predominantly due to ventricular tachycardia rather than to ventricular fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Left ventricular pseudoaneurysm complicating inferior myocardial infarction: a case report

Acquired pseudoaneurysm of the left ventricle is a very rare disorder and mostly occurs after large transmural myocardial infarction (MI) with peak creatine phosphokinase-MB levels greater than 150 IU/mL. Patients developing left ventricular (LV) pseudoaneurysm usually present with angina or heart failure symptoms. Although different imaging modalities exist, coronary angiography is the gold standard for diagnosis. Surgery is the treatment of choice for LV pseudoaneurysms detected in the first months after MI. Here we report the case of a 74-year-old woman who presented with a relatively small inferior MI due to right coronary artery occlusion and complicated by LV pseudoaneurysm.     

Combined right and left ventricular infarction: Pathogenesis and clinicopathologic correlations

An autopsy examination was made in 102 consecutive cases of fatal myocardial infarction that occurred in a coronary care unit. Thirty-five of the patients (34 percent) were found to have right ventricular infarction. All of the right ventricular infarcts were associated with transmural infarction of the posterior left ventricle or the interventricular septum, or both. The group with right ventricular infarction was compared with that without right ventricular infarction. Both groups had a predominant pattern of coronary arterial atherosclerosis consisting of severe stenosis of the proximal left anterior descending and proximal right coronary arteries with variable involvement of the left circumflex and left main coronary arteries. There was no significant difference between the two groups in severity or distribution of coronary arterial atherosclerosis. However, the group with right ventricular infarction had twice as many recent coronary arterial occlusions as did the group with left ventricular infarction and at least one recent coronary arterial lesion was present in 86 percent of those with right ventricular infarction, compared with only 30 percent of the group with left ventricular infarction. The majority of the acute coronary arterial lesions in both groups were thrombotic, but many intramural hemorrhages within atherosclerotic plaques were also found. In both groups the greatest number of recent coronary arterial occlusions was in the proximal right coronary artery, but the acute lesions were distributed throughout the coronary arterial tree.     

Right ventricular hypertrophy is an important determinant of right ventricular infarction complicating acute inferior left ventricular infarction

To explore the role of right ventricular hypertrophy and chronic obstructive pulmonary disease in the pathogenesis of right ventricular infarction, 27 consecutive patients with a first inferior left ventricular infarction were prospectively studied. Right ventricular infarction was diagnosed using established hemodynamic criteria. Right ventricular hypertrophy was defined as right ventricular free wall thickness greater than or equal to 5 mm. Patients were classified into two groups: Group I patients with right ventricular infarction (n = 15), and Group II patients without right ventricular infarction (n = 12). The ratio of forced expiratory volume over forced vital capacity (FEV1/FVC) and forced expiratory flow between 25 and 75% expired volume (FEF) as a percent of predicted values were significantly reduced in Group I versus Group II (90 +/- 5 versus 105 +/- 6% and 63 +/- 13 versus 103 +/- 15%, respectively; p less than 0.05). This was associated with increased right ventricular wall thickness (Group I 5.5 +/- 0.3 mm versus Group II 3.9 +/- 0.2 mm, p less than 0.001). Multiple logistic regression analysis demonstrated that right ventricular wall thickness was the strongest predictor of right ventricular infarction (p less than 0.0005). No significant difference was found in the site of right coronary occlusion, collateral blood supply or extent of coronary artery disease between the two groups. These findings suggest that right ventricular hypertrophy predisposes patients with acute inferior myocardial infarction to right ventricular infarction independent of the site or extent of coronary artery disease.