Donald E. Tow

Perioperative myocardial infarction after coronary artery bypass surgery. Clinical significance and approach to risk stratification.

The clinical significance of perioperative myocardial infarction (MI) after coronary artery bypass surgery is not known. Therefore, strategies for the risk stratification of these patients do not exist. This study was undertaken to define the effect of perioperative MI on prognosis after discharge from the hospital and to develop an approach to the risk stratification of these patients. Fifty-nine patients with and 115 patients without perioperative MI were observed for 30 months for the development of cardiac events (death, nonfatal MI, and admission to hospital for unstable angina or congestive heart failure). Patients with perioperative MI were significantly more likely than patients without to have a cardiac event (31% versus 12%, p less than 0.01) and multiple events (19% versus 1%, p less than 0.001). Cox regression analysis identified two independent predictors of cardiac events other than perioperative MI (relative risk, 2.7): inadequate revascularization (relative risk, 3.5) and depressed (less than 40%) postoperative ejection fraction (EF) (relative risk, 2.1). Event-free survival rate of patients with perioperative MI varied markedly depending on the number of other negative prognostic variables present. Patients with perioperative MI who were adequately revascularized and had a postoperative EF greater than 40% had an event-free survival rate similar to patients without a perioperative MI (92% versus 87%, p = NS). Patients with perioperative MI who were inadequately revascularized and had depressed postoperative EF had an event-free survival rate of 13% (p less than 0.001 versus all other subsets). Event-free survival rate was intermediate (68%) in patients with perioperative MI and with only one of the other two variables (p less than 0.001 versus other subsets). In conclusion, perioperative MI adversely affects prognosis. Patients can be stratified into low, high, and intermediate risk subsets based on a simple assessment of the adequacy of revascularization and a determination of residual left ventricular function.

The effects of large negative intrathoracic pressure on left ventricular function in patients with coronary artery disease.

Using first-pass radionuclide ventriculography, we evaluated the effects of decreases in intrathoracic pressure (Mueller maneuver [M] to −20 to −30 cm H2O) in 14 patients with and five patients without coronary artery disease (CAD) and in 12 normal control subjects. In the patients without CAD, control ejection fraction was 0.53 ± 0.06 (SEM) and control heart rate was 83 ± 6 beats/min. These did not change during M. In the patients with CAD, control ejection fraction was 0.37 ± 0.03 and heart rate was 82 ± 7 beats/min. During M, heart rate did not change, but ejection fraction decreased to 0.33 ± 0.03 (p < 0.01). Examination of regional wall motion abnormalities showed akinesis of at least one myocardial segment in nine of 14 patients with CAD, but in none of the patients without CAD, nor in any of the 12 previously studied normal subjects (retrospectively analyzed). These data are consistent with the hypothesis that the Mueller maneuver acts to increase afterload placed on the left ventricle. Furthermore, in patients with CAD, the Mueller maneuver may have induced localized myocardial ischemia or unmasked areas of preexisting marginal function.

Deep venous thrombosis in acute spinal cord injury: a comparison of 125I fibrinogen leg scanning, impedance plethysmography and venography.

Twenty acute spinal cord injury patients were surveyed for deep venous thrombosis (DVT) by 125I fibrinogen leg scanning, impedance plethysmography (IPG), and venography. Leg scanning was a more sensitive indicator of thrombotic events than IPG or venography. IPG was a reliable indicator of accumulated thrombosis. The incidence of DVT assessed by leg scanning alone was 100 per cent. Its occurrence as determined by either of the screening techniques was found to be considerably greater than those of previous reports.

Urokinase in Pulmonary Embolism

THE use of thrombolytic enzymes or their activators has been proposed as a treatment of thromboembolic diseases such as pulmonary embolism. Using streptokinase as the plasminogen activator, Johnson...

The significance of the late fall in myocardial PCO2 and its relationship to myocardial pH after regional coronary occlusion in the dog.

After acute regional coronary occlusion, myocardial tissue PCO2, as measured by mass spectrometry, rises, reaches a peak, and then gradually falls. This late fall in myocardial tissue Pco2 could be due to (1) a gradual increase in tissue blood flow (and hence improved carbon dioxide washout), (2) a gradual consumption of tissue biocarbonate, (3) a gradual reduction in the production of carbon dioxide due to progressive cellular damage, or (4) an artifact caused by the continued presence of the mass spectrometer probe in the ischemic tissue. To determine which of these four mechanisms is responsible for the late fall in myocardial tissue Pco2, we subjected 27 anesthetized open-chest dogs to 3-hour occlusion of the left anterior descending coronary artery. Both myocardial tissue Pco2 and intramyocardial hydrogen ion concentration were measured in the myocardial segment supplied by the left anterior descending coronary artery. Ten dogs (group 1) were killed after the occlusion (occlusion I), and 11 dogs (group 2) underwent reocclusion (occlusion II) at the same site after a 45-minute period of reflow. Regional myocardial blood flow was measured periodically by the intramural injection of 127Xe. Changes in myocardial tissue Pco2 and hydrogen ion concentration were related to ultrastructural changes in the tissues adjacent to the myocardial tissue Pco2 probe. Regional myocardial blood flow remained unchanged throughout the 3-hour occlusion, ruling out increased carbon dioxide washout as a cause for its late fall. Tissue hydrogen ion concentration, as measured by a new lead glass electrode, correlated well with myocardial tissue Pco2, with the reduction in regional myocardial blood flow, and with ischemic damage assessed histologically. Myocardial hydrogen ion concentration also exhibited a late fall after the occlusion, from a peak of 199.8 ± 27.8 nmol/ liter to 91.9 ± 12.1 nmol/liter (mean ± SEM). This ruled out consumption of tissue bicarbonate as the cause for the late fall in myocardial tissue Pco2. Peak rise in myocardial tissue Pco2 after occlusion II (71.2 ± 7.9 mm Hg) was significantly lower than peak myocardial tissue Pco2 after occlusion I (116.7 ± 13.9 mm Hg, P < 0.001). The difference between these latter two values, as well as the magnitude of fall in myocardial tissue Pco2 during occlusion I, related directly to the degree of histological damage observed. In six additional experiments (group 3), peak myocardial tissue Pco2 in myocardial segments supplied by normal (unoccluded) coronary arteries remained unchanged over 3 hours, and hydrogen ion concentration in segments supplied by an occluded left anterior descending coronary artery exhibited a late fall, even in the absence of a mass spectrometer probe. We conclude that, following regional coronary occlusion, there is a late fall in both myocardial tissue Pco2 and hydrogen ion concentration; this late fall probably is a reflection of progressive cellular damage which does not reverse after a 45-minute period of reflow. Myocardial tissue Pco2 and hydrogen ion concentration curves following coronary occlusion reflect the metabolic viability of the ischemic myocardium.

Assessment of the Efficacy of Interventions to Limit Ischemic Injury by Direct Measurement of Intramural Carbon Dioxide Tension after Coronary Artery Occlusion in the Dog

Although numerous interventions have been shown to exert a salutary effect on the ischemic myocardium, the severity of ischemia generally has been measured by indirect techniques. In the present investigation the effect of ischemia on intramural carbon dioxide tension (PmCO(2)) was measured directly in the open-chest, anesthetized dog with a mass spectrometer during repetitive 10-min coronary artery occlusions separated by 45-min periods of reflow; simultaneously, regional myocardial blood flow in the ischemic area was measured by (127)Xenon washout. In all dogs the increase in PmCO(2) from before to 10 min after the first occlusion (DeltaPmCO(2)) exceeded that during subsequent occlusions. In those dogs not receiving an intervention (controls), DeltaPmCO(2) during the third occlusion was similar to that during the second occlusion. When propranolol, hyaluronidase, and nitroglycerin were administered to different groups of dogs before the third occlusion, each caused significantly smaller elevations in DeltaPmCO(2) than those occurring during the control second occlusion, and the combination of all three interventions induced the smallest increase in DeltaPmCO(2). Regional myocardial blood flow rose with hyaluronidase and was unchanged with propranolol, nitroglycerin, and the three drugs in combination. In contrast to these beneficial interventions, isoproterenol infused with the third occlusion caused a higher DeltaPmCO(2) than during the control second occlusion. It is concluded, first, that interventions that modify the severity of ischemia can be evaluated by measuring intramural carbon dioxide tension; second, that propranolol, hyaluronidase, and nitroglycerin reduce ischemic injury, whereas isoproterenol increases it; and third, that the combination of propranolol, hyaluronidase, and nitroglycerin exerts an additive beneficial effect on ischemia.

Effect of Regional Hypoxia on the Distribution of Pulmonary Blood Flow in Man

In ten patients with chronic lung disease unilateral airway hypoxia was produced by having them breathe 100% nitrogen administered for seven minutes via a Carlens catheter while the other lung received 100% oxygen. The partition of pulmonary arterial blood flow between the two lungs was determined by radioisotope scanning following intravenous injection of I131 macroaggregated human serum albumin (MAA) both during bilateral air breathing and unilateral hypoxia. Unilateral hypoxia produced a 42% decrease in pulmonary blood flow to the hypoxic lung due to ipsilateral vasoconstriction. The response to N2 was greater when given to the diseased lung, suggesting that the pulmonary vascular bed of the involved lung was incapable of accepting a large increase in the proportion of the cardiac output because the vascular bed was already compromised by disease. Ventilation on the hypoxic side increased by 1.4 liters/min while there was no change on the side receiving 100% oxygen. Since unilateral hypoxia produced both a decreased blood flow and an increased ventilation, it is suggested that the lung is capable of altering regional perfusion and ventilation in a manner ideally suited to minimize the change in alveolar and pulmonary capillary oxygen tension.

Non-Q wave perioperative myocardial infarction: assessment of the incidence and severity of regional dysfunction with quantitative two-dimensional echocardiography.

Since the widespread use of hypothermic potassium cardioplegia began, marked reductions in perioperative mortality and the rate of Q wave-associated myocardial infarctions have been noted. No study to date has evaluated whether there has been an equally dramatic improvement in the incidence of postoperative myocardial infarctions unassociated with Q wave development. We used a previously validated quantitative two-dimensional echocardiographic analytic algorithm to determine the incidence and severity of regional wall motion abnormalities (RWMAs) and first-pass radionuclide ventriculography to assess deterioration in global left ventricular function in the four following groups of patients (total n = 65): (1) those with peak postoperative creatine kinase (CK)-MB levels equal to or less than the mean value for patients undergoing coronary artery bypass surgery at our institution (n = 10), (2) those with CK-MB levels between the mean and 1 SD above the mean (n = 10), (3) those with peak CK-MB levels higher than 1 SD above the mean (n = 25), and (4) those with new pathologic Q waves on the postoperative electrocardiogram (n = 20). All patients had electrocardiograms without pathologic Q waves and normal wall motion and ejection fraction by contrast ventriculography before surgery. The incidence of postoperative RWMA by two-dimensional echocardiography for groups 1 through 4 was 0%, 20%, 55%, and 89%, respectively. Percent of abnormal left ventricular segments, wall motion scores, and the deterioration in left ventricular ejection fraction as assessed by radionuclide ventriculography were similar for patients with new RWMAs whether or not new Q waves developed (p = NS for all).(ABSTRACT TRUNCATED AT 250 WORDS)

Reduced Uptake of Bone-Seeking Radiopharmaceuticals Related to Iron Excess

A suggestive relationship between the degree of iron overload and decreased skeletal uptake of phosphorus containing bone seeking radiopharmaceuticals was noted in four patients. It is postulated that iron excess may affect the organ distribution of bone seeking radiopharmaceuticals (phosphates and phosphonates) and that iron overload may account for some of the poor quality of bone scans seen clinically.

Circadian and circannual rhythm of nonfatal pulmonary embolism.

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