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.     

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 infarction: role of the moderator band artery in determining infarct size

We studied 19 patients with proximal right coronary artery occlusions associated with acute myocardial infarcts less than 30 days old. Right ventricular infarct size, determined as a percentage of right ventricular surface area, ranged from 0% to 29%. Correlation of 24 variables measuring infarct size, chamber size and coronary artery disease failed to demonstrate a significant correlation with the extent of right ventricular infarction. However, estimates of the degree of obstruction to potential collateral flow into the right coronary arterial system from the left anterior descending coronary artery, especially through the moderator band artery, showed a significant positive correlation with infarct size (p less than 0.02). Among the five patients with massive (greater than 25%) right ventricular infarction, four had significant (greater than 75%) obstruction of the left anterior descending system, resulting in potentially impaired collateral blood flow; the other patient had normal coronary arteries and embolic occlusion of the proximal right coronary artery with contraction band necrosis. The study suggests that collateral flow to the right ventricular myocardium, especially through the moderator band artery, protects against massive infarction in the presence of proximal right coronary artery occlusion.     

Myocardial infarction with ventricular aneurysm in a newborn with normal coronary arteries

Myocardial infarction is very rare in a neonate with structurally normal coronary arteries. We report a case in which myocardial infarction was complicated by a left ventricular aneurysm in the setting of normal coronary arteries. There was an associated muscular ventricular septal defect. All defects were diagnosed by cross-sectional echocardiography, angiography and myocardial scintigraphy.     

Subendocardial stress in pre‐eclampsia

A primigravida 26‐year‐old woman who had developed pre‐eclampsia with malignant hypertension at 30 weeks of gestation suffered acute myocardial infarction two days postpartum. Electrocardiogram demonstrated diffuse ST‐segment depression suggestive of subendocardial ischemia. Echocardiography demonstrated focal asymmetric left ventricular hypertrophy, with a characteristic “basal septal bulge”, and a left ventricular mid‐cavitary gradient of 51 mmHg. Coronary angiography revealed normal coronary arteries and vascular flow. Peripartum acute myocardial infarction is rare and portends a high mortality. However, to date, only one case of acute myocardial infarction associated with asymmetric left ventricular hypertrophy and pre‐eclampsia has been described in the literature.     

An unusual cause of right ventricular myocardial infarction

A unique case of right ventricular myocardial infarction complicating an acute inferior-posterior myocardial infarction in a patient with a single left coronary artery is described. The clinical, electrocardiographic, and hemodynamic features of right ventricular myocardial infarction and the angiographic patterns of anomalous single coronary arteries are reviewed.     

Coronary reserve, left ventricular function, and coronary risk factors in patients with myocardial infarction, but normal coronary arteries (author's transl)

In 5 patients with angiographically normal coronary arteries and previous myocardial infarction (left ventricular a- or dyscinesia), measurement of coronary reserve revealed normal values. On average, patients with myocardial infarction and normal coronary arteries were younger than patients with angiographically proven obstructive coronary lesions (p less than 0,001), and did not exhibit a rise in coronary risk factors. These results suggest that in some cases myocardial infarction is due to acute, completely reversible occlusion or severe stenosis of larger coronary arteries without morphological or functional defects of coronary arteries detectable later on.     

Effects of left ventricular hypertrophy on the coronary circulation

Many laboratories have provided evidence to support the concept that LV hypertrophy is associated with many significant coronary perfusion abnormalities. The decreased coronary flow reserve in the presence of LV hypertrophy is implicated as the mechanism of angina in patients with aortic stenosis and normal coronary arteries. The abnormal subendocardial autoregulation found in dogs may have important implications for the abrupt treatment of hypertension in patients with LV hypertrophy. The marked increase in mortality and the wavefront of infarction in dogs with hypertension and LV hypertrophy may have striking clinical implications for the salvage of myocardium in patients with chronic hypertension and LV hypertrophy during acute myocardial infarction.     

Vascular and cardiac contractile reserve in the dog heart with chronic multiple coronary occlusions.

Nineteen mongrel dogs survived chronic occlusion of the left circumflex and of the right coronary artery without infarction due to the timely development of a collateral circulation. Only 38 per cent of the conductance of the arteries before occlusion was restored by collateral vessels. In these animals and in 15 control dogs with normal coronary arteries myocardial contractility, contractility reserve, and myocardial blood flow were studied. The same was done in dogs with chronic coronary artery occlusion after aortocoronary bypass. Myocardial blood flow was determined woth the tracer microsphere technique. Contractility reserve was tested and defined as isovolumetric left ventricular pressure and dp/dt max with norepinephrine infusion and cross-clamping of the aorta. Contractile reserve was not significantly different between normal dogs and dogs with chronic coronary artery occlusion before and after aortocoronary bypass. Myocardial blood flow during control conditions was homogenously distributed in all three groups studied. The ratio of blood flow to the endocardium and the epicardium was not significantly different from inity. Coronary reserve was determined at peak reactive hyperemia following a 20 second period of coronary artery occlusion, with ongoing norepinephrine infusion. Under these conditions subendocardial fow in normal dogs rose by a factor of 7.9 while subepicardial flow increased 7.4 times. In dogs with chronic occlusion of two coronary arteries the increase of myocardial flow was nonnomogenous; subendocardial flow to areas supplied by a normal coronary artery rose by a factor of 7.0 while subepicardial flow increased 5.7 times control. Subendocardial collateral flow rose by a factor of 2.4 and subepicardial collateral flow increased 3.5 times control. In normal dogs norepinephrine alone did not result in maximal coronary flow but only 57 per cent thereof. Dogs with chronic coronary occlusion, however, required the entire coronary reserve in areas that were supplied by a normal coronary artery, whereas areas supplied by collaterals became ischemic. Opening of an aortocoronary bypass restored normal flow to previously ischemic areas, and reduced the flow to areas supplied by a normal artery. With the bypass open no differences existed between normal dogs and those with two occluded coronary arteries. We conclude that the norepinephrine-stimulated contractile reserve of hearts with chronic coronary occlusion was comparable to that of normal hearts; however, norepinephrine forced these hearts to spend the entire flow reserve of the remaining normal artery while producing ischemia in collateral-dependent areas. The same dose of norepinephrine did not require the entire flow reserve of normal dogs.     

Subendocardial stress in pre-eclampsia

A primigravida 26-year-old woman who had developed pre-eclampsia with malignant hypertension at 30 weeks of gestation suffered acute myocardial infarction two days postpartum. Electrocardiogram demonstrated diffuse ST-segment depression suggestive of subendocardial ischemia. Echocardiography demonstrated focal asymmetric left ventricular hypertrophy, with a characteristic “basal septal bulge”, and a left ventricular mid-cavitary gradient of 51 mmHg. Coronary angiography revealed normal coronary arteries and vascular flow. Peripartum acute myocardial infarction is rare and portends a high mortality. However, to date, only one case of acute myocardial infarction associated with asymmetric left ventricular hypertrophy and pre-eclampsia has been described in the literature.     

Coronary spasm and diffuse coronary vasoconstriction responsible for transient left ventricular insufficiency

A 52 year old patient presenting with spontaneous anginal chest pain for 4 days was admitted to hospital for a more intense and prolonged chest pain associated with signs of left ventricular failure (gallop, pulmonary crepitations, hypoxemia). Coronary angiography showed marked septal hypokinesia and spontaneous localised spasm of the left anterior descending and marginal arteries with a variable degree of luminal narrowing of the other segments of these two arteries and of the right coronary artery. These changes regressed after intracoronary injection of molsidomine. The signs of left ventricular failure disappeared in 48 hours. The wall motion abnormality, monitored by 2D echocardiography, regressed slowly over 3 days. On the other hand, the electrocardiogram, which showed anterior wall subendocardial ischaemia with prolongation of the QTc interval during the spasm, remained abnormal for a long time. Therefore, in the absence of organic heart disease, coronary spasms associated with vasoconstriction can induce a sufficiently severe and durable alteration of left ventricular function to create clinical signs of cardiac failure and profound and prolonged ST-T wave changes on the electrocardiogram.     

Noninvasive assessment of left and right ventricular filling in myocardial infarction with a two-dimensional Doppler echocardiographic method

Inflow characteristics of left and right ventricular filling were assessed in 40 patients with myocardial infarction and in 10 normal subjects by pulsed Doppler echocardiography. Patients with myocardial infarction were subdivided into four groups, focusing on the involvement of right ventricular and septal branches of the coronary arteries. Group I consisted of 11 patients with anterior infarction who showed an obstructive lesion of the proximal left anterior descending branch involving the first septal perforator with a patent right coronary artery. Group II consisted of 10 patients with inferior infarction who showed an obstructive lesion of the proximal right coronary artery involving the right ventricular branch. Group III consisted of 12 patients with both anterior and inferior infarction who showed obstructive lesions of both the proximal left anterior descending branch and the right coronary artery involving the right ventricular branch. Group IV consisted of seven patients with lateral infarction who showed an obstructive lesion of the diagonal branch or branches of the circumflex coronary artery with a patent left anterior descending branch and right coronary artery. Three measurements were performed from the transmitral and transtricuspidal inflow velocity patterns to assess the left and right ventricular diastolic behaviors. These measurements were: acceleration half-time, deceleration half-time of early diastolic rapid inflow, and the ratio of the peak velocity of early diastolic rapid inflow to that of the late diastolic inflow due to the atrial contraction. Impaired diastolic filling of the left ventricle compensated by enhanced left atrial contraction was observed in patients with myocardial infarction from groups I, II, III and IV.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of acute, transient coronary occlusion on global and regional right ventricular function in humans.

OBJECTIVES. The aim of this study was to investigate the changes in right ventricular function during acute coronary occlusion produced by inflating a coronary angioplasty balloon catheter. BACKGROUND. Alterations in right ventricular function are well known to occur in patients with acute myocardial infarction or ischemic cardiomyopathy. However, the changes in right ventricular function resulting from acute, transient coronary occlusion of each of the major coronary arteries have been scantily studied, perhaps because of serious limitations of currently available technology. METHODS. A newly designed, mobile, multiwire gamma camera, in combination with generator-produced tantalum-178, affords high count rate first-pass radionuclide angiography and is thus ideal for studying right ventricular function at the bedside. Accordingly, 46 patients underwent first-pass radionuclide angiography at baseline and during transient coronary occlusion induced by a coronary angioplasty balloon catheter. RESULTS. A significant, albeit modest, decrease in global right ventricular ejection fraction occurred during occlusion of the left anterior descending (from 42.9 +/- 9.3% to 39 +/- 8.7%, p < 0.05) and left circumflex (from 44 +/- 9.1% to 38.8 +/- 7.9%, p = 0.03) coronary arteries, but diagonal artery occlusion caused no significant change in right ventricular ejection fraction. Occlusion of the right coronary artery proximal (but not distal) to the acute marginal branch caused a significant decrease in right ventricular ejection fraction (from 42.6 +/- 4.7% to 35.7 +/- 7.2%, p < 0.01). Although occlusion of the left anterior descending, left circumflex and proximal right coronary arteries all caused significant deterioration in regional right ventricular function, only proximal right coronary occlusion caused right ventricular dilation (p < 0.005). CONCLUSIONS. Significant impairment of right ventricular function occurs during transient occlusion of the left anterior descending, left circumflex and proximal right coronary arteries, but only occlusion of the latter causes acute right ventricular dilation, probably as a result of ischemia.     

Two cases of dilated cardiomyopathy complicated by left ventricular aneurysm

This report describes two patients with dilated cardiomyopathy associated with angiographically proven left ventricular aneurysm. There was no apparent history of myocardial infarction and coronary arteries were angiographically normal in both cases.     

Acute myocardial infarction with diminutive right coronary artery and obstructive hypertrophic cardiomyopathy without significant coronary stenoses

Focal tissue abnormalities consistent with regional ischemia have been reported in patients with hypertrophic cardiomyopathy (HCM). Coronary microvascular dysfunction has been also reported to be present in patients with HCM despite normal epicardial coronary arteries. Moreover, it has been demonstrated that in the case of HCM and idiopathic left ventricular hypertrophy, hypoplastic coronary arteries as diminutive vessels are present and that obstructive hypertrophic cardiomyopathy is associated with enhanced thrombin generation and platelet activation. Previously, it has been described an acute myocardial infarction in a young athlete with non-obstructive hypertrophic cardiomyopathy and normal coronary arteries. We present a case of an acute myocardial infarction with diminutive right coronary artery and obstructive hypertrophic cardiomyopathy without significant coronary stenoses. To our knowledge, this is the first report of an acute myocardial infarction with diminutive right coronary artery and obstructive hypertrophic cardiomyopathy without significant coronary stenoses.     

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.     

An uncommon cause of myocardial infarction

A 73 year-old lady with hypertension and chronic atrial fibrillation (AF) developed chest pain followed by ventricular fibrillation (VF) cardiac arrest. Her electrocardiogram post-cardioversion revealed inferior ST-elevation myocardial infarction (MI). Her coronary arteries were angiographically normal. Contrast-enhanced cardiac magnetic resonance(CE-CMR) demonstrated both an inferior subendocardial infarction and left atrial (LA) appendage thrombus suggesting cardioembolism as the most likely cause of her presentation.     

Subtle left ventricular asynergy with completely obstructed coronary arteries

The phenomenon of apparently normal angiographic left ventricular wall motion in the presence of ≥ 1 completely obstructed coronary artery was investigated in 16 patients with coronary artery disease (CAD) by quantitative phasic biplane cineangiography. Angiographic contours were digitized at quarterly intervals throughout ejection and 9 areas of motion were measured in both right and left anterior oblique planes. Normal values were derived from 18 other patients who had normal coronary arteries and normal left ventricular function. Areas of asynergy undetected when quantitative analysis was applied only at end-systole in the right anterior oblique plane were found in 12 of the 16 patients with CAD: in 2 patients by end-systolic analysis in the left anterior oblique plane and in 10 patients by phasic analysis of both planes. Of 19 asynergic areas 18 corresponded to sites of high-grade CAD. All patients had angina pectoris, but only 5 had clinical or electrocardiographic evidence of prior infarction.     

Right ventricular infarction mimicking extensive anterior infarction

Two patients with inferior infarction complicated by right ventricular infarction are presented. Both manifested electrocardiographic changes involving the anterior chest leads with initial S-T segment elevation followed by loss of R waves and the development of QS complexes mimicking anterior infarction. Cardiac catheterization showed right coronary artery occlusion with normal left coronary system and anterior wall motion in each case. Radionuclide angiocardiography showed dilated poorly contracting right ventricles. The ECG changes of "anterior infarction" in these patients were therefore due solely to right ventricular injury.     

Right ventricular infarction complicating left ventricular infarction secondary to coronary heart disease: Frequency, location, associated findings and significance from analysis of 236 necropsy patients with acute or healed myocardial infarction

Right ventricular infarction associated with left ventricular infarction was identified by gross examination at necropsy in 33 (14 percent) of 236 patients with transmural myocardial infarction. Right ventricular infarction occurred exclusively as a complication of posterior left ventricular infarction. Associated right ventricular infarction occurred in none of the 97 patients with isolated anterior wall infarction of the left ventricle, but in 33 (24 percent) of the 139 patients with posterior left ventricular infarction. Transmural infarction of the posterior ventricular septum was an additional prerequisite for right ventricular infarction. Of the 139 patients with infarction of the posterior left ventricular wall, 74 had no transmural infarction of the ventricular septum and none of these 74 had associated right ventricular infarction. In contrast, of the 65 patients with infarction of the posterior left ventricular wall and transmural infarction of the ventricular septum, 33 (50 percent) had associated right ventricular infarction.

Among the 33 patients with right ventricular infarction, the infarct was limited to the posterior right ventricular free wall in 27 (82 percent); in the other 6 patients (18 percent) it extended to involve the anterolateral right ventricular free wall. Among patients with a posterior left ventricular infarct, those with a right ventricular infarct had right ventricular dilatation nearly three times (P < 0.05) more frequently than the patients without a right ventricular infarct. Comparison of the same two groups disclosed no differences in the patients' age, sex, extent of coronary arterial luminal narrowing, right ventricular hypertrophy, right ventricular thrombi or duration of symptoms of myocardial ischemia.

Hemodynamic data in four patients with a right ventricular infarct disclosed previously reported characteristic hemodynamics of right ventricular infarction in only one patient. Recognition of right ventricular infarction is important because it implies specific therapy, namely, aggressive volume administration. Clinical evidence of posterior left ventricular infarction and right ventricular dilatation should arouse strong suspicion of associated right ventricular infarction.