Norman B. Ratliff

Combined right and left ventricular infarction: Pathogenesis and clinicopathologic correlations☆

Abstract 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.

The natural history of right coronary arterial occlusion in the pig: Comparison with left anterior descending arterial occlusion☆

Abstract Gradual occlusion of the right coronary artery in the farm pig produces a much lower mortality rate than occlusion of the left anterior descending artery. The rate and extent of collateral vessel development in these 2 arteries after the gradual occlusion of each were compared in the pig using selective coronary cineangiograms. Serial studies were performed over 42 days after placement of an ameroid constrictor on the right coronary artery in 24 pigs (RCA group) and on the left anterior descending artery in 27 pigs (LADA group). Despite similar rates of occlusion, collateral vessels developed earlier in pigs in the RCA group. With partial occlusion collaterals were seen in 75 percent of those in the RCA group and in 33 percent of those in the LADA group. After total occlusion, the contralateral vessel was completely opacified at 1, 2, 3 and 4 weeks in 40, 71, 87 and 100 percent, respectively, of animals studied in the RCA group, compared to 8, 20, 40 and 100 percent of animals in the LADA group. Histologic evidence of myocardial infarction, although present in all animals, was more extensive in animals in the LAPA group. All myocardial infarctions noted were limited to the left ventricle although blood supply to the right ventricle is almost exclusively from the right coronary artery. The difference in the rapidity and extent of collateral vessel development may be related to the dissimilarity in pressure and mass between the right and left ventricles, and it may explain the lower mortality rate, smaller left ventricular infarction and absent right ventricular infarction following occlusion of the right coronary artery.

Collateral vessel development after right ventricular infarction in the pig

Abstract 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.

Myocardial oxygen metabolism and myocardial blood flow in dogs in hemorrhagic shock.

We have studied the interrelations of myocardial oxygen metabolism and myocardial blood flow in hemorrhagic shock. Myocardial blood flow was measured by the 133Xe-washout method in closed-chest anesthetized dogs while the dogs were breathing either room air at ambient pressure or oxygen at high pressure. In animals with normal blood pressure, oxygen at high pressure produced a consistent decrease in myocardial blood flow from a mean of 70 ml/100 g/min to a mean of 43 ml/100 g/min, with a proportionate decrease in myocardial O2 consumption. In animals in hemorrhagic shock, oxygen at high pressure induced no change in myocardial blood flow but increased myocardial O2 consumption from a mean of 5.9 ml/100 g/min to a mean of 7.4 ml/100 g/min. When the animals in hemorrhagic shock breathed room air again at ambient pressure following oxygen at high pressure, the myocardial blood flow increased from a mean of 40 ml/100 g/min to a mean of 51 ml/100 g/min. The myocardial O2 consumption did not change. We conclude that with decreasing blood pressure a baseline of myocardial blood flow may be reached, so that a further decrease no longer occurs in response to hyperoxia. However, the control of myocardial blood flow in shock is an active process responsive to complex positive control mechanisms that may be altered and studied experimentally.

The Effects of Hemorrhagic Shock on the Heart

It has become abundantly clear that shock produced by hemorrhage, as well as by other means, is a multisystem disease involving cells of many organs (1). It is apparent, therefore, that no one organ system need be implicated as the “weak link” which, if strengthened, would prevent irreversibility after transfusion since there are many alternative vicious cycles that can lead to death. However, it is our contention that the heart is significantly damaged during the course of a shock episode, and that this damage is severe enough to lead to a functional defect. There is impressive physiologic and anatomic evidence that this probably is a major contributing factor to irreversibility in most instances.