D. G. Mathey

Non surgical coronary artery recanalization in acute transmural myocardial infarction.

In 41 consecutive patients with an acute transmural myocardial infarction (AMI) admitted within 3 hours after the onset of symptoms, we tried to recanalize the occluded coronary artery by an intracoronary infusion of streptokinase (SK) (2000 units/min). SK infusion was preceded by (1) an intracoronary injection of 0.5 mg nitroglycerin to rule out coronary artery spasm, (2) an attempt to recanalize the vessel mechanically with a flexible guidewire, and (3) an intracoronary injection of plasminogen (500 units) to increase the efficacy of the subsequent SK infusion. Coronary angiography revealed a total coronary artery occlusion in 39 patients and a subtotal occlusion in two patients. In 30 patients (73%), the occluded coronary artery was successfully recanalized within 1 hour (mean 29 ± 15 minutes), resulting in prompt contrast filling of the previously occluded vessel. An arteriosclerotic stenosis always remained at the site of the occlusion. Nitroglycerin opened the occluded coronary artery in one patient, contrast injection in seven patients and guidewire perforation in four of the 15 patients, in whom it was attempted. In 18 patients the occluded coronary artery was recanalized by intracoronary SK infusion alone. After the initial opening of the occluded coronary artery, subsequent SK infusion markedly reduced the degree of stenosis and visible thrombi disappeared. Clinically, recanalization was associated with significant relief of ischemic chest pain. None of the successfully recanalized patients died, including three patients with cardiogenic shock. Recanalization, however, did not prevent myocardial infarction, as shown by new Q waves and/or R-wave reduction in 24 of the 30 patients and by the rise in serum CPK with an early peak, indicating CPK washout by coronary artery reperfusion. Repeat angiography 7-21 days later revealed a patent coronary artery in 12 of 15 successfully recanalized patients. The left ventricular ejection fraction had significantly improved, from 37

Left ventricular relaxation and filling pattern in different forms of left ventricular hypertrophy: An echocardiographic study☆

Abstract To study left ventricular relaxation and filling in different forms of left ventricular hypertrophy, echocardiograms of the left ventricle in 24 patients with hypertrophic obstructive cardiomyopathy and in 24 patients with chronic left ventricular pressure overload (due to aortic stenosis in 6 and to severe arterial hypertension in 18) were analyzed by computer and compared with those of 28 normal subjects. The relaxation time index (minimal left ventricular dimension to mitral valve opening) was 13 ± 15 ms in normal subjects. This index was prolonged in patients with cardiomyopathy (93 ± 37 ms) and overload (66 ± 31 ms). During the interval from minimal left ventricular dimension to mitral valve opening both groups with left ventricular hypertrophy showed a marked increase in left ventricular dimension of 4.0 ± 2.2 mm and 3.0 ±1.8 mm, respectively, which was significantly greater (p The rapid filling phase and the increase in dimension during this period were significantly reduced in hypertrophic obstructive cardiomyopathy and chronic pressure overload. In contrast to findings in the patients with cardiomyopathy, in those with pressure overload the reduced increase in left ventricular dimension during the rapid diastolic filling period was compensated for by a greater dimensional increase due to atrial contraction, resulting in a normal end-diastolic dimension. These data indicate that significant prolongation of isovolumic relaxation is seen in different forms of left ventricular hypertrophy and is often associated with an abnormal diastolic filling pattern.

Incomplete lysis of thrombus in the moderate underlying atherosclerotic lesion during intracoronary infusion of streptokinase for acute myocardial infarction: quantitative angiographic observations.

Thrombolytic recanalization of the obstructed coronary lumen was studied in 32 patients receiving intracoronary streptokinase for 60 to 90 min during acute myocardial infarction. The process was viewed at high arteriographic magnification and was quantified with computer-assisted measurements from repeated single-plane views. The variability of the method for this application was 0.15 to 0.18 mm on minimum diameter estimates. Structural details were seen that are not commonly appreciated at conventional magnification. The recanalized lumen appears to form along an interface between the thrombus and the vessel wall, progressively enlarging its minimum arteriographic diameter to 0.65 +/- 0.24 mm (+/- 1 SD) at the end of the short-term infusion of streptokinase reflecting a final percent stenosis of 77 +/- 10%. In nine infarct lesions found patent 5 +/- 3 weeks later, the recanalized lumen further improved an average of 0.34 mm in minimum diameter (p less than .005) and 13% stenosis (p less than .01). A thin film of contrast medium surrounding the obstructing thrombus faintly defined the boundaries of the original atherosclerotic lumen in all but two cases. The original stenosis measured 1.25 +/- 0.32 mm in minimum diameter and 56 +/- 14% stenosis when first visualized; it was unchanged throughout the course of infusion of streptokinase. In five patients catheterized 10 +/- 12 weeks before their infarction, the original stenosis averaged 1.15 +/- 0.22 mm in the preinfarct angiogram, as compared with 1.17 +/- 0.23 mm in its faintly defined form during thrombolytic therapy (p = NS). In 10 cases, this original lesion was less than a 50% stenosis, and in 21 cases less than 60%.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of interventions in salvaging left ventricular function in acute myocardial infarction: A study of intracoronary streptokinase

The ability of intracoronary streptokinase (STK) infused early in acute myocardial infarction (MI) to salvage left ventricular (LV) function was studied in 52 patients who underwent contrast angiography immediately after STK and 6 +/- 7 weeks later. Ten nonrevascularized patients had no lysis or reocclusion. Of 42 patients with thrombolysis, 22 with optimal reperfusion underwent coronary artery bypass grafting (CABG) to prevent rethrombosis (STK + CABG group) and 20 did not (STK group). Motion was measured at 100 chords around the left ventricle and expressed in standard deviations (SD) from the normal mean. Hypokinesia was computed as the mean motion of chords in the infarct artery territory and hyperkinesia on the opposite wall was similarly computed. Hypokinesia improved greater than or equal to 1 SD/chord in 9 STK + CABG patients (41%), 8 STK patients (30%) (p = not significant versus STK + CABG) and 0 nonrevascularized patients. However, the ejection fraction did not change because it was normal in acute MI despite severe hypokinesia due to hyperkinesia on the opposite wall, and a subsequent decrease in hyperkinesia masked significant improvement in hypokinesia. It is concluded that regional wall motion must be measured to adequately assess the effect of therapeutic interventions on LV function. Early thrombolysis in acute MI results in improved LV function. The main benefit of CABG is to prevent rethrombosis.

Intravenous urokinase in acute myocardial infarction

To achieve reperfusion early, an intravenous bolus of 2 million units of urokinase was administered in 50 patients with transmural acute myocardial infarction (AMI) 1.8 +/- 2.5 hours after the onset of symptoms. Coronary angiography performed 1.1 +/- 0.6 hours after urokinase therapy revealed patent coronary arteries in 30 patients (60%), with no significant difference between those with anterior and those with inferior AMI. Reocclusion occurred in only 1 of 24 patients restudied. Failure to achieve reperfusion was not related to the degree of systemic fibrinolytic activity, which was equally high in patients who did and those who did not achieve reperfusion, as evident from serially obtained fibrinogen measurements (77 +/- 52 vs 84 +/- 24 mg/dl, difference not significant). Plasmin activity, measured serially from 15 minutes to 24 hours after urokinase in 7 patients, was maximal at 15 minutes and undetectable after 3 hours. Wall motion at the infarct site measured from contrast ventriculograms was significantly better at follow-up only in patients in whom reperfusion was achieved and who received urokinase within 2 hours after the onset of symptoms as compared with patients in whom reperfusion was not achieved (-1.2 +/- 1.4 vs -2.4 +/- 0.9 standard deviations from normal, p less than 0.05). Peak serum creatine kinase level was significantly lower in patients in whom reperfusion was achieved than in those in whom it was not or those who had rethrombosis (802 +/- 763 vs 1,973 +/- 1,071 U/liter, p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of verapamil on left ventricular isovolumic relaxation time and regional left ventricular filling in hypertrophic cardiomyopathy

Hypertrophic obstructive and nonobstructive cardiomyopathy are often associated with an abnormal prolonged left ventricular isovolumic relaxation time and a disturbed left ventricular filling pattern [1–5]. Recent experimental studies revealed that calcium antagonists may improve impaired left ventricular relaxation caused by ischemia or hypoxia [6, 7]. Based on these experimental results, it was the purpose of the present study to examine whether the impaired left ventricular relaxation in patients with obstructive and nonobstructive hypertrophic cardiomyopathy can be improved by intravenous application of verapamil.

Factors that determine recovery of left ventricular function after thrombolysis in patients with acute myocardial infarction.

The coronary and ventricular angiograms of 47 patients with acute myocardial infarction in whom reperfusion was achieved by intracoronary streptokinase were quantitatively analyzed to determine the factors that affect recovery of regional left ventricular function after reperfusion. Hypokinesis in the infarct region was measured by the centerline method and expressed in terms of standard deviations (SDs) from normal. Severity of coronary artery stenosis was measured quantitatively. Hypokinesis showed more significant improvement after thrombolysis in patients with minimum stenosis diameter of greater than 0.4 mm than in those with severe residual stenosis, i.e., stenosis producing a minimum diameter of 0.4 mm or less (1.0 +/- 1.3 SD/chord, n = 31, vs 0.0 +/- 0.9 SD/chord, n = 7; p less than .05). Improvement in hypokinesis was greater in patients who received thrombolytic therapy within 2 hr than in those treated later (2.1 +/- 1.1, n = 8, vs 0.7 +/- 1.0 SD/chord, n = 28; p less than .001). These results indicate that angiographic reperfusion alone may not be sufficient: reperfusion must provide adequate flow and be achieved early to salvage myocardial function.

Prehospital thrombolysis in acute myocardial infarction

The benefit and risk of prehospital thrombolysis for acute myocardial infarction (AMI) were evaluated in a double-blind randomized trial. Patients presenting less than 4 hours after symptom onset received 2 million units of urokinase as an intravenous bolus either before (group A, n = 40) or after (group B, n = 38) hospital admission. The mean time interval from onset of symptoms to thrombolytic therapy was 85 +/- 51 minutes in group A and 137 +/- 50 minutes in group B (p less than 0.0005). In 91% of the patients, thrombolytic therapy was administered less than 3 hours after symptom onset. Complication rates during the pre- and in-hospital period were low and did not differ between groups. Three patients died (1 in group A, 2 in group B) from reinfarction 7 to 14 days after admission. Left-sided cardiac catheterization before discharge revealed a patency rate in the infarct-related artery of 61% in group A and 67% in group B (difference not significant). Global left ventricular function and regional wall motion at the infarct site did not differ significantly between group A and B (ejection fraction 51 +/- 10%, n = 28 vs 53 +/- 14%, n = 28; wall motion -2.3 +/- 1.3 vs -2.2 +/- 1.1 standard deviation, respectively). Also, peak creatine kinase did not differ significantly (838 +/- 634 U/liter in group A vs 924 +/- 595 U/liter in group B). Prehospital thrombolysis using a bolus injection of urokinase has a low risk when performed by a trained physician with a mobile care unit. The saving of 45 minutes in the early stage of an acute infarction through prehospital thrombolysis did not appear to be important for salvage of myocardial function.

Lysis of left ventricular thrombi with urokinase.

In 16 patients with recent myocardial infarction (3 to 12 week old) and with large left ventricular thrombi systemic thrombolysis with urokinase was performed. Left ventricular thrombi were diagnosed by two-dimensional echocardiography; in all patients the mural thrombus was located in the area of recent myocardial infarction. Each of three patients suffered an embolic episode before the initiation of thrombolytic therapy and the episode caused a stroke in one. Urokinase was infused intravenously at a rate of 60,000 U/hr for 2 to 8 days in combination with intravenous heparin (200 units/kg X 12 hr). Left ventricular thrombi were successfully lysed in 10 of 16 patients, as determined by two-dimensional echocardiography. In four of the six remaining patients only partial thrombolysis was achieved and in two thrombolytic treatment failed. There was no evidence of embolic events during thrombolysis in any of the 16 patients. The success of thrombolysis seemed to depend on the age of the thrombus: the thrombus was dissolved in eight of nine patients undergoing thrombolysis within 4 weeks of the acute myocardial infarction vs in two of seven patients receiving treatment later (p = .057). The presence of a left ventricular aneurysm or depressed left ventricular function also appeared to reduce the likelihood of successful thrombolysis. All patients were discharged on oral anticoagulants. At 6 months follow-up (n = 9) no recurrence of left ventricular thrombus was found. These results show that left ventricular thrombi can be safely lysed by intravenous urokinase. However, for better definition of the risk and benefit of this new therapy further investigation is necessary.

Measurement of regional wall motion from biplane contrast ventriculograms: a comparison of the 30 degree right anterior oblique and 60 degree left anterior oblique projections in patients with acute myocardial infarction.

The value of performing biplane vs single plane analysis of regional wall motion from contrast ventriculograms was determined in 102 patients who received thrombolytic therapy and who underwent biplane ventriculography during acute myocardial infarction (n = 67), at follow-up more than 2 weeks later (n = 80), or both (n = 45). Hypokinesis in the infarct region and hyperkinesis in the noninfarct region were measured by the centerline method in the respective artery territories, which were defined from the data of 62 patients with single-vessel disease and were expressed in units of standard deviations from the mean of 32 normal subjects. Hypokinesis was more severe and extended over a longer segment of the left ventricular contour when measured in the right anterior oblique (RAO) projection in thrombosis of the left anterior descending coronary artery (LAD) but more severe and extensive in the left anterior oblique (LAO) projection in circumflex stenosis. Hyperkinesis opposite the LAD or the circumflex was greater in the LAO projection. In patients with thrombosis of the right coronary artery, wall motion abnormalities were similar in the two projections. Thus the evaluation of hypokinesis caused by acute coronary thrombosis and of the effect of therapeutic interventions in salvaging function can be adequately evaluated from single-plane 30 degree RAO ventriculograms, except in the small minority of patients with circumflex thrombosis.