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Biomedical subjects

M L Marcus

Publications and source records attributed to M L Marcus.

At least 109 records · Page 6Linked to original sources

Absence of functioning alpha-adrenergic receptors in mature canine coronary collaterals.

To determine if mature coronary collateral vascular smooth muscle contains functioning alpha-adrenergic receptors, we studied 13 dogs, 6-10 months after circumflex ameroid occlusion. Regional myocardial blood flow was measured with radioactive microspheres in a blood-perfused heart preparation at constant aortic pressure (80 mm Hg). Normal zone resistance was calculated as aortic pressure divided by normal zone flow, and transcollateral resistance was calculated as aortic pressure minus circumflex pressure distal to the ameroid constrictor divided by coronary collateral flow. Flow and resistance were measured during adenosine vasodilation before and during graded doses of a constant infusion of the alpha-adrenergic agonist methoxamine (n = 6) or the alpha 2-adrenergic agonist clonidine (n = 7). In the hearts that received methoxamine, normal zone resistance increased from a control of 0.29 +/- 0.06 to 0.39 +/- 0.06 mm Hg X min/ml per 100 g (resistance units) during infusion of 10(-5)M methoxamine (p less than 0.05). In contrast transcollateral resistance averaged 0.24 +/- 0.02 resistance units under control conditions and did not change during methoxamine infusion. In the hearts that received clonidine, normal zone resistance averaged 0.24 +/- 0.03 resistance units and increased to 0.39 +/- 0.07 resistance units (p less than 0.05) with the highest dose of clonidine administered (10(-5) M). Transcollateral resistance averaged 0.17 +/- 0.03 resistance units during control conditions and did not change with clonidine infusion. In separate studies isometric tension development by the left anterior descending and coronary collateral vessels was examined in organ baths. The left anterior descending coronary artery demonstrated dose-dependent constriction to phenylephrine (peak response 22 +/- 5% of the response to 100 mM KCl). Clonidine produced weak constrictor responses in the left anterior descending coronary artery (5 +/- 2.5% maximal KCl response). In contrast, neither phenylephrine nor clonidine produced responses in mature collaterals. We also examined responses of mature collateral vessels to nonadrenergic agonists. In the vascular ring preparation the mature collaterals developed tension in the presence of KCl (2.3 +/- 0.9 g), prostaglandin F2 alpha (16 +/- 18% of the KCl responses), and vasopressin (90 +/- 30% of the KCl response). In adenosine-vasodilated hearts, pharmacologic doses of vasopressin caused a two-fold increase in transcollateral resistance. Thus, these studies performed on intact hearts and isolated vascular rings demonstrate that mature coronary collaterals do not contain functioning alpha-adrenergic receptors.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic alpha-Agonists↗

Potentiation of vasoconstrictor responses to serotonin in the limb of atherosclerotic monkeys.

Vasoconstrictor responses to serotonin and norepinephrine were examined in: normal cynomolgus monkeys, atherosclerotic monkeys that were fed atherogenic diet for 3-5 years and hypercholesterolaemic but non-atherosclerotic monkeys that were fed atherogenic diet for 4-5 months. Serotonin decreased total hindlimb resistance in normal and hypercholesterolaemic monkeys, but increased total resistance in atherosclerotic monkeys. There was a greater than 10-fold increase in constrictor responses of large arteries to serotonin in atherosclerotic compared with normal and hypercholesterolaemic monkeys. In contrast, responses to norepinephrine were not increased in atherosclerotic monkeys. Thus, atherosclerosis greatly potentiates constrictor responses to serotonin in large arteries of the limb. This potentiation appears to be somewhat selective for serotonin, as it is not observed with norepinephrine.

Animals↗

Application of Doppler technology to studies of the coronary circulation.

Presently available Doppler technology has allowed us to substantially increase our understanding of the regulation of the coronary circulation in humans. New technologic developments in this area promise to further enhance our understanding of the operational characteristics of the coronary circulation in patients in normal and pathologic states.

Angina Pectoris↗

Effect of high-dose cyclophosphamide and total-body irradiation on left ventricular function in adult patients with leukemia undergoing allogeneic bone marrow transplantation.

Protocols used to prepare patients with leukemia for bone marrow transplantation have the potential for cardiac toxicity due to high-dose cyclophosphamide and total-body irradiation. We have reported one regimen, combining cytarabine (5 mg/kg), cyclophosphamide (90 mg/kg), and total-body irradiation (900 cGy), which is relatively effective in the treatment of leukemia. To assess cardiac effects of this treatment regimen, we performed serial echocardiography and radionuclide ventriculography in 28 patients with leukemia (age range, 18-48 years; mean, 31; 21 males) undergoing allogeneic bone marrow transplantation. No significant change in left ventricular fractional minor axis shortening or increase in left ventricular diastolic dimension was seen with weekly echocardiography. At an average of 77 days (range, 28-358) after transplant, repeat radionuclide ventriculography in 17 patients revealed no significant change in resting left ventricular ejection fraction compared to that on admission to the hospital (58% +/- 6.8% vs 56% +/- 8.0% SD; P = not significant). In seven of these 17 patients (41%), resting ejection fraction fell between baseline and discharge (from mean of 60% to 50%). Resting ejection fraction in four of these patients (23% of the entire group) fell into the abnormal range (from mean of 56% to 44%; lowest, 41%). Ten patients also had exercise radionuclide ventriculography and all had normal responses (greater than 5% increase with exercise) pre- and post-transplant. We conclude that this effective bone marrow transplantation regimen has little apparent short-term cardiac toxicity in the majority of patients; since a few patients do exhibit a deterioration in left ventricular function, continued cardiac surveillance is probably indicated in posttransplant patients.

Adolescent↗

Assessing the physiological significance of coronary obstruction in man.

At present, it is widely assumed that the physiological significance of a coronary obstruction can be assessed by measuring percent stenosis on a coronary arteriogram. This assumption is being challenged by physiological measurements of coronary reserve performed in patients at open heart surgery with a Doppler technique. These physiological studies have shown a poor correlation between coronary reserve and percent stenosis. Although stenoses at the ends of the spectrum (less than 10% or greater than 90% diameter narrowing) have expected effects on coronary reserve, stenoses of intermediate severity (10-90%) do not accurately predict coronary reserve in the individual vessel involved. Studies with quantitative angiography indicate that diffuse coronary atherosclerosis, undetected by angiography, is probably the dominant explanation for why percent stenosis does not accurately predict the physiologic significance of coronary obstructions in man. Because the 'gold standard' (percent stenosis) utilized for decades to assess the physiologic significance of coronary obstructive lesions has been seriously challenged, development of other more sophisticated approaches to this problem should be encouraged.

Animals↗

Myocardial infarct size threshold for two-dimensional echocardiographic detection: sensitivity of systolic wall thickening and endocardial motion abnormalities in small versus large infarcts.

This study evaluated the ability of 2-dimensional echocardiography to detect myocardial infarcts of varying sizes. Echocardiography was performed in 29 closed-chest, conscious dogs 2 days after circumflex coronary artery occlusion, and the ultrasonic recordings were analyzed for regional abnormalities in either wall thickening or endocardial motion. Acute myocardial infarct (AMI) size and extent were assessed by morphologic examination. In 5 dogs, coronary occlusion failed to produce AMI; in these dogs wall thickening analysis showed no abnormalities (100% specificity), and endocardial motion analysis yielded 1 false-positive result (80% specificity). In 24 dogs an AMI developed; infarcts larger than 18% of left ventricular mass uniformly resulted in echocardiographically detectable contraction abnormalities. When the AMI was small (1 to 6% of left ventricular mass) and primarily subendocardial, the sensitivity of echocardiography was poor: Only 3 of 10 of the dogs with a small AMI had abnormalities by wall thickening, and only 1 of 10 by endocardial motion. Thus, in this canine model of AMI, 2-dimensional echocardiography was insensitive to small, subendocardial AMI. If this is so in humans as well, it is a potential limitation of the clinical use of echocardiography in the detection of AMI.

Animals↗

Effects of chronic hypertension on vasa vasorum in the thoracic aorta.

The outer layers of the thoracic aorta receive substantial blood flow through vasa vasorum within the aortic wall. Flow delivered via these channels is functionally important because medial necrosis occurs when vasa vasorum are ligated. If flow through vasa vasorum is limited in chronic hypertension, this could contribute to medial necrosis and, perhaps, aortic dissection. In these experiments, flow and conductance in vasa vasorum were assessed in twelve awake dogs with renal hypertension (arterial pressure = 127 +/- 4 mmHg [mean +/- SE]) and nine normotensive controls (arterial pressure = 100 +/- 3 mmHg [P less than 0.001]). At rest, blood flow delivered via vasa vasorum to the thoracic aorta was similar in hypertensive and normotensive dogs (5.2 +/- 0.9 and 4.8 +/- 0.4 ml . min-1 X 100 g-1 respectively). Thus, in hypertensive dogs, conductance of the vasa vasorum decreased to maintain flow constant. During maximal dilatation induced by iv adenosine (4.7 mumol . kg-1 per min) flow delivered via vasa vasorum increased by 100% in both hypertensive and normotensive dogs. Calculations of maximum conductance indicate that vasodilator capacity was decreased by 67% in vasa vasorum of hypertensive dogs. These data suggest that vasodilator capacity of vasa vasorum in the thoracic aorta is limited in chronic hypertension. This abnormality could contribute to the pathogenesis of medial necrosis and aortic dissection in hypertensive patients.

Adenosine↗

Effects of coronary and extravascular pressure on intramyocardial and epicardial blood velocity.

In open-chest anesthetized dogs we measured phasic coronary blood velocity in an epicardial artery (left anterior descending), a small epicardial artery (within 0.5 cm before penetration into the myocardium), and an intramyocardial artery (septal) during changes in perfusion pressure and extravascular pressure. Circumflex artery diameter was also measured during pressure changes to directly assess vascular compliance. At low and normal arterial pressures (less than 125/86 mmHg) and during aortic insufficiency, the phasic character of blood flow velocity in the large epicardial arteries was markedly different from that in the small epicardial and septal arteries: there was retrograde systolic blood flow velocity in the septal artery and small epicardial artery, whereas antegrade blood flow velocity persisted in the left anterior descending artery. At pressures greater than 150/106 mmHg, the differences in the phasic character of blood flow velocity in the left anterior descending artery from that in the septal artery and small epicardial artery were small and decreased as aortic pressure increased. At pressures greater than 125 mmHg, the cross-sectional area change per millimeter of mercury was approximately three times less than at pressures between 30 and 75 mmHg, indicating decreased coronary compliance at the higher pressures. Increasing extravascular pressure in the septum (right ventricular hypertension) greatly increased retrograde systolic blood flow velocity in the septal artery (P less than 0.05). However, right ventricular bypass (0 right ventricular pressure) did not alter the phasic nature of blood flow velocity in the septal artery. From these results we confirmed that epicardial capacitance is inversely related to distending pressures.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

The effect of cardiac hypertrophy on the coronary collateral circulation.

We have previously shown that dogs with renal hypertension and left ventricular hypertrophy have larger infarcts (per risk area size) than do control animals. A potential explanation for this is that collateral resistance is higher in these dogs. Paradoxically, previous postmortem studies in human hearts with left ventricular hypertrophy have suggested that coronary collaterals are actually increased in this condition. To test the hypothesis that left ventricular hypertrophy is associated with alterations in coronary collateral resistance, studies were performed in dogs with renal hypertension and left ventricular hypertrophy and in patients with aortic valvular disease at the time of cardiac surgery. With an isolated, adenosine-vasodilated, blood-perfused cardiac preparation, collateral and normal zone pressure-flow relationships were established by means of radioactive microspheres in nine dogs with renal hypertension and left ventricular hypertrophy and in 17 controls. Collateral resistance calculated from these pressure-flow relationships were similar in both groups (4.0 +/- 0.7 in dogs with renal hypertension and left ventricular hypertrophy and 3.9 +/- 0.4 mm Hg/ml/min/100 g in controls). In addition, normal zone resistance was not different between groups (transmural resistances 0.17 +/- 0.01 in controls and 0.18 +/- 0.02 in dogs with renal hypertension and left ventricular hypertrophy. In five patients with aortic valve disease, left ventricular hypertrophy, and normal coronary arteries and in six patients without left ventricular hypertrophy who had normal left anterior descending coronary arteries, a 7 MHz suction-mounted echo transducer was used to monitor systolic wall thickening during transient occlusions of the left anterior descending artery at the time of cardiac surgery. Because noncollateralized myocardium ceases to contract promptly after coronary occlusion, this approach provides an indirect index of collateral perfusion. Twenty seconds after the onset of coronary occlusion, systolic thickening had markedly decreased in both groups (15 +/- 10% of control values in nonhypertrophied hearts and 10 +/- 10% in hearts with left ventricular hypertrophy; p = NS between groups). Thus the severity of contraction abnormality induced during transient coronary occlusion in these two groups of patients was similar, suggesting that the degree of severity of ischemia was comparable between the two groups. We conclude that collateral resistance is not altered by hypertension and left ventricular hypertrophy and that left ventricular hypertrophy in patients is not associated with functional evidence of an enhanced collateral circulation.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Transluminal, subselective measurement of coronary artery blood flow velocity and vasodilator reserve in man.

Assessment of coronary blood flow and the vasodilator reserve capacity of individual coronary arteries in the catheterization laboratory has been hampered by methodologic limitations. We have developed and validated a small Doppler catheter that can subselectively measure phasic coronary blood flow velocity (CBFV). In seven anesthetized calves, CBFV was varied from 0.1 to 5.7 times control CBFV. Changes in mean CBFV measured intraluminally by catheter in the left anterior descending and left circumflex arteries were similar to those measured simultaneously with an epicardial Doppler probe on the surface of the same vessel (n = 85, r = .95, slope = 1.04) and to changes in coronary sinus flow (n = 69, r = .97, slope = 1.06) measured with timed venous collections. Identical maximal coronary reactive hyperemic responses with the catheter present and absent in the artery being studied demonstrated that coronary obstruction by the catheter was minimal. Safety studies in six additional calves demonstrated that the catheter caused small changes in coronary endothelial permeability. Histologic studies revealed no endothelial denudation or thrombus formation. Stable phasic recordings of coronary blood flow velocity have been obtained in 58 of 70 patients studied. One of the 70 patients studied had abrupt coronary occlusion probably related to catheter-induced vasospasm. In 10 normal patients, intracoronary meglumine diatrizoate increased CBFV to 3.5 times that at rest (range 2.8 to 5.0). CBFV rose 5.0-fold after an intravenous infusion of dipyridamole (range 3.8 to 7.0). In each patient, dipyridamole produced greater vasodilation than meglumine diatrizoate. The time- and dose-response characteristics to dipyridamole infusion were heterogeneous, underscoring the advantage of continuous on-line measurement of CBFV in the measurement of vasodilator reserve. This method of measuring CBFV and assessing vasodilator reserve in the catheterization laboratory should facilitate studies of the coronary circulation in man.

Animals↗

Determination of left ventricular mass in dogs with rapid-acquisition cardiac computed tomographic scanning.

The development of left ventricular hypertrophy in patients with heart disease often has far-reaching clinical implications with respect to overall morbidity and mortality. Approaches used to assess left ventricular mass include electrocardiography, echocardiography, contrast ventriculography, single photon-emission tomography, and conventional computed tomography. However, all of these modalities suffer from some major draw back that precludes widespread application to all patients. In this study we assessed the accuracy of determinations of left ventricular mass in 22 dogs by rapid-acquisition (50 msec) computed axial tomography (RACAT), an ultrafast computed tomographic (CT) instrument. Electrocardiographically triggered, end-diastolic, short-axis cardiac scans were obtained from apex to base during administration of intravenous iodinated contrast. Myocardial edges were determined for each tomographic scan by two methods: the regional half-contour method (the CT density half way between that of the left ventricular myocardium and adjacent ventricular cavities or lung) and "interactive plateau thresholding" of the cardiac borders. Left ventricular mass by RACAT was calculated as the sum of the mass of each individual scan from apex to base (modified Simpson's rule). Postmortem left ventricular mass ranged from 58 to 160 g. The correlation between true left ventricular mass and tomographically determined mass was excellent (r = .99), with the slope and y intercept not statistically different from 1 and 0, respectively. The standard error of the estimate was 4.1 g. Interobserver and intraobserver variability for determining left ventricular mass demonstrated excellent agreement (r = .99 and r = .99, respectively). We conclude that quantitative assessment of left ventricular mass can be accurately and reproducibly performed in dogs by rapid acquisition CT scanning. It is likely that this technique will be readily transferable to the clinical settings and prove to be an important method for quantifying left ventricular mass in patients.

Animals↗

Removal of the endothelium potentiates canine large coronary artery constrictor responses to 5-hydroxytryptamine in vivo.

Recent studies in isolated epicardial coronary artery rings have shown that the endothelium modulates vasomotor responses to certain endogenous neurohumoral agents. It is not known whether the endothelium plays a role in large coronary vasoregulation in the intact coronary circulation. Accordingly, we examined effects of endothelial removal on vasoconstrictor responses of the proximal coronary artery in anesthetized adult mongrel dogs. The left anterior descending artery was perfused at 100 mm Hg with arterial blood from a pressurized reservoir. Coronary diameter was measured continuously with 7-MHz sonomicrometer crystals attached to the adventitia of the artery. Fifteen minutes after mechanical disruption of the endothelium with a balloon-tipped catheter, baseline diameter was unchanged from a control value of 2.60 +/- 0.13 mm (mean +/- SE, n = 17). Endothelial denudation resulted in a dose-dependent potentiation of the constrictor response to intracoronary 5-hydroxytryptamine (1-50 micrograms/min, n = 8). With the endothelium intact, a 5 micrograms/min infusion of 5-hydroxytryptamine reduced diameter by 24 +/- 14 micron, while a 50 micrograms/min dose reduced diameter by 54 +/- 25 micron. After endothelial removal, the decrease in diameter averaged 74 +/- 18 microns at 5 micrograms/min and 132 +/- 29 micron at 50 micrograms/min, indicating a 10-fold increase in the sensitivity to 5-hydroxytryptamine. The constrictor responses to angiotensin II (1 and 5 micrograms/min, n = 7) and phenylephrine (1-5 micrograms/min, n = 7) were not altered by endothelial removal. Thus, endothelial removal selectively potentiates the constrictor responses to 5-hydroxytryptamine in the intact coronary circulation of the dog.

Angiotensin II↗

Thyroxine-induced left ventricular hypertrophy in the rat. Anatomical and physiological evidence for angiogenesis.

We examined anatomical and physiological responses of the left coronary vascular system to thyroxine-induced myocardial hypertrophy. Wistar-Kyoto rats (1 and 5 months old) were administered thyroxine (0.25 mg/kg per day) or the saline vehicle (sham-treated controls) for 2 months. At the ages of 3 and 7 months, each group of animals was used for one of three experimental protocols: determination of numerical capillary density in perfusion-fixed hearts, measurement of coronary reactive hyperemic responses following a 20-second coronary occlusion (peak-to-resting blood flow velocity) as an index of coronary reserve, and assessment of myocardial perfusion under resting conditions and during maximum coronary dilation (dipyridamole infusion) for the calculation of minimum coronary resistance per unit weight of the left ventricle or minimum coronary resistance of the total left ventricle. In both groups of thyroxine-treated animals, the left ventricular weight-to-body weight ratio increased by 35-40%. Capillary density of the 3- and 7-month-old Wistar Kyoto controls was 4467 +/- 352 (mean +/- SEM) and 4029 +/- 143 capillaries/mm2, respectively, but was increased significantly in the thyroxine-treated animals to 6052 +/- 409 capillaries/mm2 (3-month) and 4654 +/- 201 capillaries/mm2 (7-month). In both age control groups, the peak-to-resting blood flow velocity ratio was about 2.2. This index of coronary reserve was not changed in the thyroxine-treated animals. Myocardial perfusion measurements were limited to the 7-month-old animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effects of long-term cardiac hypertrophy on coronary vasodilator reserve in SHR rats.

The effects of long-term left ventricular (LV) hypertrophy on coronary vascular reserve have not been extensively investigated. To test the hypothesis that the duration of LV hypertrophy may modulate coronary vascular reserve, a newly developed pulsed Doppler flowmeter was used to compare the characteristics of coronary reactive hyperemia in Wistar Kyoto (WKY) and spontaneously hypertensive (SHR) rats. The data suggest that coronary reactive hyperemic responses in the rat are markedly different from those in larger animals and humans, e.g., peak/rest blood flow velocity ratio and the repayment/debt area ratio were 30 to 50% of those observed in larger laboratory animals. Because minimal coronary vascular resistance is similar in the rat and larger animals, the relatively high myocardial oxygen consumption at rest and consequent high myocardial blood flow at rest probably account for the alteration of coronary reactive hyperemia in the rat. In SHR rats, the characteristics of coronary reactive hyperemia decreased during developing (3-month-old) and peak (7-month-old) LV hypertrophy compared with those in their age-matched WKY controls. However, in 12-month-old SHR rats with stable LV hypertrophy, the coronary reactive hyperemic response was similar to that of 12-month-old WKY rats. Mean arterial pressures were significantly elevated in each of the 3 SHR groups. These data suggest a significant decrement in coronary vascular reserve during actively developing and peak LV hypertrophy, but the decrement disappears during stabilized hypertrophy. These studies suggest that the duration of LV hypertrophy may modulate the interaction between pathologic increases in cardiac mass and growth of the coronary vasculature.

Animals↗

Coronary reserve in volume-induced right ventricular hypertrophy from atrial septal defect.

To assess coronary reserve in patients with right ventricular (RV) hypertrophy secondary to volume overload, the quantitative characteristics of coronary reactive hyperemia were examined in 20 patients with a large atrial septal defect (ASD). The control group consisted of 13 patients who had undergone elective cardiac surgery for abnormalities that did not involve the right ventricle or its blood supply. Coronary blood flow velocity was measured in RV branches of the right coronary artery at cardiac surgery. Echocardiographic measurements of RV diameter in ASD and in control patients (2.3 +/- 0.2 and 1.1 +/- 0.2 cm, respectively, p less than 0.05) documented the presence of substantial RV enlargement in patients with ASD. In patients with ASD and in control subjects, a 20-second coronary occlusion produced maximal coronary dilation. After release of a 20 second coronary occlusion, the peak-to-resting velocity ratio in ASD and in control patients was 3.1 +/- 0.2 and 5.5 +/- 0.1, respectively (p less than 0.05). The 50% decrease in the ratio of peak-to-resting coronary blood flow velocity, a measure of relative coronary reserve, in patients with ASD suggests that coronary reserve is compromised in volume-induced RV hypertrophy. These studies support the concept that in humans, volume-induced RV hypertrophy substantially decreases coronary reserve.

Adolescent↗

Influence of baseline ejection fraction and success of thrombolysis on mortality and ventricular function after acute myocardial infarction.

The efficacy of streptokinase (STK) thrombolytic therapy was prospectively evaluated in 77 consecutive patients presenting within 9 hours of onset of acute myocardial infarction. Serial left ventricular (LV) ejection fraction (EF) was assessed by radionuclide ventriculography, initially (acute) and at 1 month (late). The role of initial LVEF was examined by comparing patients with an acute LVEF greater than or equal to 50% (type I) with those with LVEF less than 50% (type II). Sixty-five patients (84%) had total coronary occlusion and received STK. Initial successful reperfusion was achieved in 34 patients (52%), but repeat angiograms at 10 to 14 days revealed persistent patency in only 27 patients. Within the type I and type II classification, 2 patient subgroups were compared: Group A had successful and persistent thrombolysis and group B had initial failure of thrombolysis or in-hospital reocclusion. There was no significant change in global LVEF in any group from acute to 1 month follow-up: group IA--acute EF = 56 +/- 2% (mean +/- standard error of the mean), late EF = 55 +/- 2% (p = not significant [NS]); group IB--acute EF = 58 +/- 1%, late EF = 55 +/- 2% (NS); group IIA--acute EF = 35 +/- 2%, late EF = 4 +/- 4%, (NS); group II B--acute EF = 36 +/- 2%, late EF = 41 +/- 3% (NS). No patient with an acute EF greater than or equal to 50% died, i.e., group IA patients (n = 7) or group IB patients (n = 13).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Systemic markers of fibrinolysis after unsuccessful intracoronary streptokinase thrombolysis for acute myocardial infarction. Does nonreperfusion indicate failure to achieve a systemic lytic state?

Reasons for the failure of intracoronary streptokinase (STK) to result in coronary thrombolysis were examined in 45 patients with acute myocardial infarction presenting with angiographic evidence of total coronary occlusion. In 25 patients (group A), clot lysis was initially successful; in 20 (group B), reperfusion was unsuccessful. The STK dosage in group A ranged from 84,000 to 310,000 units (mean 188,000 +/- 12,000); STK dosage in group B ranged from 160,000 to 360,000 units (mean 267,000 +/- 11,000 [p less than 0.05]). Before therapy, levels of fibrin degradation products and serum fibrinogen were normal in all patients. After intracoronary STK, fibrin degradation products and serum fibrinogen levels changed similarly in both groups. Eight-five percent of patients in group B had evidence of a systemic fibrinolytic state. These data suggest that higher doses of STK administered in the same manner are unlikely to result in an increased reperfusion rate. Systemic hematologic markers of fibrinolysis are not helpful in explaining the success or failure of intracoronary thrombolysis.

Coronary Angiography↗