Dicumarol: Its action,clinical use and effectiveness as an anticoagulant drug

Dicumarol is a potent and valuable anticoagulant drug. When used properly it appears to prevent intravascular thrombosis in almost all patients. There is considerable and unpredictable variation in sensitivity to dicumarol among different patients. Dosage of dicumarol must be guided by the effect produced in each patient as indicated by the degree and duration of prothrombin deficiency which develops and is indicated by determinations of the concentration of prothrombin in the blood. It is unwise to use dicumarol unless adequate facilities for determining the prothrombin time are available. If the prothrombin is kept between 10 and 30 per cent of normal by administration of dicumarol, thrombosis will almost certainly be prevented and serious bleeding is very unlikely to occur. The action of dicumarol is delayed. When a rapid anticoagulant effect is desired concurrent heparinization is necessary for the first few days. We have found that dicumarol has prevented fatal pulmonary embolism and recurrence or extension of venous thrombosis in patients who have had postoperative nonfatal pulmonary embolism or thrombophlebitis. There is some incomplete evidence to the effect that it will prevent peripheral thrombosis, pulmonary embolism and further coronary thrombosis in patients who have had acute myocardial infarction. Dicumarol with preliminary heparinization is valuable in the treatment of acute arterial occlusion of the extremities. It has also been used safely in patients in whom thrombophlebitis and pulmonary embolism complicated the puerperium and various diseases, in patients with idiopathic recurrent thrombophlebitis and in those with chronic occlusive arterial disease. While statistical confirmation is lacking, it is our impression that in many of these patients thrombosis and embolism have been prevented by administration of dicumarol.     

Follow-up catheterization of patients with myocardial infarction during coronary artery bypass surgery.

Of 197 consecutive patients having aortocoronary bypass grafts over a 30 month period, 38 (19 per cent) had ECG evidence of myocardial infarction. The infarctions occurred more commonly in patients receiving multiple grafts. The infarctions were usually in areas supplied by grafted vessels. The infarctions occurred most often in the inferior wall, even when multiple vessels were grafted. Eleven patients with intraoperative infarction have had repeat postoperative coronary arteriograms. Seven had all grafts patent; three of these patients had hypokinesis of the infarcted wall. Four of the 11 patients had one or more occluded grafts; three of these patients had an area of hypokinesis. We conclude that intraoperative myocardial infarction is a common problem in aortocoronary bypass surgery and is not necessarily caused by graft occlusion.     

The subsequent course and prognosis in coronary thrombosis: An Analysis of 287 Cases

The records of 287 cases of coronary thrombosis have been studied with respect to the clinical course of the disease from the time of the first attack. Approximately 85 per cent of these cases were found in men and 15 per cent in women.An analysis of the age incidence at the time of the first attack discloses the fact that in one-third of all the cases the first attack occurred before the fifty-first year, and in three-fourths of the cases before the sixty-first year. It seems evident therefore that coronary thrombosis must be regarded as essentially a disease of early middle life rather than of elderly life as it is usually held to be.Evidence of an antecedent arterial hypertension was found in 34 per cent of the cases; of syphilis in 14 per cent, and of diabetes in 10 per cent.Of the 287 patients studied 117 are known to be living and 142 to have died.The immediate mortality in the first attack was 16.2 per cent.Of 117 patients who recovered satisfactorily from the first attack, 75 per cent were in good health at the end of one year; 56 per cent at the end of two years; 21 per cent at five years and 3.4 per cent at ten years. One patient remained in good health for seventeen years and died in a second attack eighteen years after the first.In 62 per cent of the patients the first attack supervened, without antecedent circulatory symptoms, in persons who had no reason to doubt the integrity of the heart.A single attack only of thrombosis is recorded in 67 per cent of all the patients; two attacks occurred in 24 per cent; three attacks in 4 per cent and from four to seven attacks in 5 per cent.Of the patients having but a single attack, one-half are living and one-third are in good health.Among the patients having two or more attacks the time interval between the first and the second attack was less than one year in half of the cases and in the other half varied from one to eighteen years.Signs of arterial embolism appeared 49 times among 42 patients. Twenty-eight of the embolic attacks involved the systemic arteries and 21 the pulmonary artery.Although the immediate mortality in attacks of coronary thrombosis is higher when the initial symptoms are severe than when they are mild, yet almost one-third of the patients who recovered from the attack had symptoms of very severe character.     

Hemorrhagic myocardial infarction associated with aortocoronary bypass revascularization.

Experimentally, hemorrhage and extension of myocardial infarction occur commonly when there is reperfusion after coronary artery occlusion. To investigate this hazard in a clinical setting, we compared the histopathologic picture of myocardial infarction in 44 patients who had undergone aortocoronary bypass: 14 (Group I) had myocardial infarction that predated aortocoronary bypass by 1 to 7 days; 13 (Group II) had infarction 1 to 14 days after the surgery; and 17 (Group III) had infarction 15 to 90 days postoperatively. All 44 patients had two or more coronary arteries with luminal narrowing of more than 75 per cent and patent vein grafts to arteries supplying areas of infarction. Hemorrhagic infarcts were present in 57 per cent of patients (eight of 14) in group I and 38 per cent of patients (five of 13) in Group II, contrasting with 6 per cent of patients (one of 17) in Group III (P < 0.005 and P < 0.05, respectively). In hemorrhagic infarcts, the extravasated blood formed irregular intramural dissecting tracts beyond the area of infarction, and foci of myocardial necrosis were present in the border zones. Infarcts affected more than 50 per cent of the left ventricular muscle in 64 per cent of cases of hemorrhagic infarction and in 13 per cent of cases of nonhemorrhagic infarction (P < 0.05). The prevalence of hemorrhagic infarction after revascularization may account for the high mortality of evolving and perioperative myocardial infarction associated with aortocoronary bypass, and this finding militates against wholesale immediate revascularization in patients who have uncomplicated myocardial infarction.     

Revascularization in the acute phase of myocardial infarction. Study of left ventricular function in the 3d week and 6th month

27 patients with primary myocardial infarction are treated, in the first 6 hours, with intravenous thrombolysis with immediate coronary angiographic control showing a patent artery in 76 p. cent of the cases. The treatment is completed with intracoronary thrombolysis (5 times) and transluminal angioplasty (6 times), enabling to obtain a patency rate of 88 p. cent. The overall left ventricular function is evaluated at D21 and in the 6th month (M6). Among anterior infarctions, those treated during the first three hours have a better ejection fraction (EF) at D21 than those treated later (40.3 p. cent +/- 6 versus 33.2 p. cent +/- -NS); this functional benefit is confirmed at M6 (42.8 p. cent +/- 12 versus 30.6 p. cent +/- 8; p less than 0.06). On the contrary, among inferior infarctions, the EF is comparable at D21 and M6 regardless of the early nature of the treatment. One patient died prematurely from a cerebral vascular accident which occurred during the thrombolysis. These results are in favor of a significant myocardial salvation in anterior infarctions revascularised at an early stage and of an active approach in order to obtain the most complete possible revascularisation.     

Acute myocardial infarction with normal and near normal coronary arteries Documentation with coronary arteriography within 12 1/2hours of the onset of symptoms in two cases (three episodes)

Three instances (in two patients) of acute myocardial infarction associated with arteriographically normal or near normal coronary arteries are reported. One patient with a lateral infarction had a normal coronary arteriogram and hypokinesia of the lateral wall. Another patient had two infarctions: (1) a transmural inferior-lateral infarction associated with occlusion of the most distal segment of the posterior descending branch of the right coronary artery, and (2) a transmural anterior-lateral-superior infarction associated with occlusion of the most distal segment of the left anterior descending coronary artery. Neither occlusion was consistent with the extent of infarction. Although coronary arteriography was performed as early as 12 1/2, 3 3/4 and 11 2/3hours, respectively, after the onset of symptoms of infarction in these three instances, the pathophysiologic features of the infarctions are obscure. Temporary occlusion of an epicardial coronary artery by spasm or platelet aggregates, or both, is suggested as a possible mechanism of the acute event.     

Acute myocardial infarction with normal and near normal coronary arteries: Documentation with coronary arteriography within of the onset of symptoms in two cases (three episodes)

Three instances (in two patients) of acute myocardial infarction associated with arteriographically normal or near normal coronary arteries are reported. One patient with a lateral infarction had a normal coronary arteriogram and hypokinesia of the lateral wall. Another patient had two infarctions: (1) a transmural inferior-lateral infarction associated with occlusion of the most distal segment of the posterior descending branch of the right coronary artery, and (2) a transmural anterior-lateral-superior infarction associated with occlusion of the most distal segment of the left anterior descending coronary artery. Neither occlusion was consistent with the extent of infarction. Although coronary arteriography was performed as early as , and , respectively, after the onset of symptoms of infarction in these three instances, the pathophysiologic features of the infarctions are obscure. Temporary occlusion of an epicardial coronary artery by spasm or platelet aggregates, or both, is suggested as a possible mechanism of the acute event.     

Coronary angioplasty in unstable angina. Immediate and short-term results

We report the results of percutaneous transluminal coronary angioplasty (PTCA) in 67 consecutive patients with unstable angina. Twenty patients had new onset (less than 2 months) angina, 33 patients had crescendo angina and 14 had early postinfarction angina. Fifty-one patients had one-vessel disease, 12 patients had two-vessel disease and two patients had three-vessel disease; two patients had a stenosis of a venous graft. In cases with multivessel disease, we performed only the dilatation of the ischaemia-related vessel identified by morphologic features of coronary lesion and electrocardiographic changes during chest pain. The procedure was successful in 54 cases (80.6%). Seven patients (10.4%) had major complications. Emergency coronary artery bypass graft surgery was performed in 6 cases (8.9%) because of occlusion of the left anterior descending artery; despite emergency operation one patient died and two patients sustained a myocardial infarction. One patient had occlusion of the right coronary artery and inferior myocardial infarction. In all patients in whom angioplasty was successful unstable angina disappeared. At 6 months follow-up there were no infarctions or deaths but 14 of 42 patients (33%) had recurrent angina. Restenosis occurred in 16 of 33 patients (48%) who had repeat coronary angiography. Four patients with recurrence of unstable angina had repeat angioplasty; it was successful in 3 cases. One patient died of refractory cardiac arrest. The mortality rate of 71 procedures performed in 67 patients was 2.8% (2/71) and the overall myocardial infarction rate was 4.2% (3/71).(ABSTRACT TRUNCATED AT 250 WORDS)     

Ischemic myocardial injury during coronary artery surgery

ECG's and serum levels of SGOT, LDH, and CPK were examined during the postoperative period in 50 patients with angina pectoris who had myocardial revascularization procedures. ECG signs of acute myocardial infarction appeared in 34 per cent and changes compatible with acute ischemic injury were seen in 10 per cent. Elevation of SGOT exceeding 90 units occurred in 32 per cent of 50 patients, and LDH levels over 900 units occurred in 24 per cent. In patients with ECG evidence of post-operative infarction or ischemia, 50 per cent had abnormal SGOT levels and 55 per cent had abnormal LDH levels. In 16 patients with SGOT levels exceeding 90 units, 69 per cent had ECG evidence of acute infarction or ischemia. Two patients died following surgery and acute myocardial infarction was demonstrated in both at autopsy. Relief of angina occurred in one patient who developed a myocardial infarct following internal mammary implantation. A follow-up angiogram revealed no effective communication of the implant with myocardial vessels. Acute myocardial infarction is a frequent complication of coronary artery surgery as determined by serial ECG's. In this study, approximately 50 per cent of these patients had diagnostic elevations of SGOT or LDH.     

Complications of coronary arteriography: a follow-up report.

A nationwide survey of complications due to coronary arteriography during 1973--74 yielded responses from 176 hospitals (89,079 coronary arteriograms). The overall mortality rate was 0.14% (brachial, 0.12%; femoral, 0.16%). In the brachial group, the mortality rate was three times as high for non-heparinized as for heparinized patients. In institutions performing fewer than 100 examinations per year, the combined incidence of death, myocardial infarction, and cerebral embolism was five times higher than in institutions performing more than 400 examinations per year. Left main coronary artery or three-vessel disease was present in most patients who died of the procedure. Compared to a previous survey of 1970--71, there was a profound decrease in significant complications (including death, myocardial infarction, and cerebral embolism) and entry site complications such as thrombosis. A reduction in mortality with the femoral technique since 1971 was not accounted for by heparinization and may reflect increasing experience with the method and shorter angiographic times.     

A phonocardiographic study of the heart sounds in acute coronary occlusion

A phonocardiographic analysis employing microphones of different frequency filtering and transmission range was made of the heart sounds in seventy-eight cases of acute coronary occlusion and in 100 normal control subjects. The results were correlated with the clinical findings.The first heart sound was absolutely diminished in amplitude in 24 per cent and relatively to the second sound in 54 per cent of the patients with acute coronary occlusion. This diminution in amplitude affected the central group of high-frequency vibrations and was attributed to the change in the physical character of the infarcted left ventricle and possibly, in the first few days of illness, to the lowered intraventricular pressure following acute myocardial infarction.Occasionally the second sound at the apex is increased to an absolute as well as a relative value.An auricular sound was present in 83 per cent of cases of coronary occlusion compared to 38 per cent in normal subjects. In one-third of the cases of coronary occlusion the auricular sound was accentuated and formed presystolic gallop rhythm. This never occurred in normal subjects. Accentuation of the auricular sound was probably the result of the increased intra-auricular pressure following ventricular infarction. It was practically always associated with heart failure.A third sound occurred in 47 per cent of the cases of coronary occlusion as compared to 12 per cent in normal subjects. The high incidence in the former was attributed to the decreased tonus of the infarcted ventricular muscle. In 9 per cent of the cases the third sound appeared accentuated and produced protodiastolic gallop rhythm. Heart failure was invariably associated with it.Superimposition of the auricular and third sounds of normal or accentuated amplitude occurred in 6 per cent of cases, forming summation gallop. This type of gallop rhythm was also associated with heart failure.Clinical heart failure was present in 63 per cent of the cases of coronary occlusion. It occurred predominantly in those who presented a first sound of diminished amplitude (88 per cent) and gallop rhythm (95 per cent). It was much less common in those with an unimpaired first sound (33 per cent). This emphasizes not only the close relationship between impaired heart sounds and heart failure but also the serious import of a diminished first heart sound and gallop rhythm.Gallop rhythm may be present before signs of heart failure are apparent.The impairment of the first heart sound following coronary occlusion is often permanent and may be the only persistent sign following recovery. It thus may be of diagnostic significance.     

Pathology of hearts after aortocoronary saphenous vein bypass grafting for coronary artery disease, studied by post-mortem coronary angiography.

A detailed pathological study was made in 10 patients dying up to 13 months after aortocoronary saphenous vein bypass grafting for coronary atherosclerosis. The coronary arteries and vein grafts were investigated by injection with a radio-opaque mass, radiography, dissection, and histology. The report is to some extent historical since the patients died during a period when the operation was first being introduced into two cardiothoracic hospitals. About 80 operations were performed during the time the 10 deaths occurred, a mortality of 12-5 per cent (including cases followed up to 13 months after operation). Seven of the patients were operated on for intractable angina and 3 with a view to aneurysmectomy. All the patients selected for operation were severely disabled despite medical treatment. The main cause of death was extremely severe coronary artery disease and its effects on the left ventricle; in one case, over two-thirds of the left ventricle had been destroyed by infarction before operation. Other causes or contributing causes of death were pulmonary embolism, myocardial infarction complicating angiography (ostial stenosis), and cerebral damage. Ten of the 14 vein grafts (71%) were patent at necropsy. A free flow of injection medium usually occurred between patent grafts and coronary arteries. Thrombosis of a graft was thought to have contributed to death in 3 patients, but not in a fourth who died of pulmonary embolism. Since thrombosis of grafts was usually secondary to poor run-off blood into severely atheromatous coronary arteries, this was also an indirect effect of the advanced coronary arterial disease. In one case, thrombosis followed severe chronic intimal thickening of a graft in place for 13 months. The study of these deaths emphasizes that in some patients the pathological changes in the coronary arteries and left ventricle are too severe for them to benefit from surgery. Vein grafts cannot be expected to distribute blood effectively through grossly narrowed coronary arteries. In addition, when a large part of the left ventricle is infarcted or scarred, it is almost certain that improving the blood supply by grafting will not result in significant regeneration of cardiac muscle. Since the time when this study was made, there have been few deaths among the many vein graft operations subsequently carried out in the hospitals involved. The two most important factors thought responsible for the improvement are the selection of cases more suitable for surgery by continued improvement of diagnostic techniques, and also the employment of more radical surgical procedures in the form of coronary endarterectomy and the insertion of more grafts per patient.     

Pathology of hearts after aortocoronary saphenous vein bypass grafting for coronary artery disease, studied by post-mortem coronary angiography.

A detailed pathological study was made in 10 patients dying up to 13 months after aortocoronary saphenous vein bypass grafting for coronary atherosclerosis. The coronary arteries and vein grafts were investigated by injection with a radio-opaque mass, radiography, dissection, and histology. The report is to some extent historical since the patients died during a period when the operation was first being introduced into two cardiothoracic hospitals. About 80 operations were performed during the time the 10 deaths occurred, a mortality of 12-5 per cent (including cases followed up to 13 months after operation). Seven of the patients were operated on for intractable angina and 3 with a view to aneurysmectomy. All the patients selected for operation were severely disabled despite medical treatment. The main cause of death was extremely severe coronary artery disease and its effects on the left ventricle; in one case, over two-thirds of the left ventricle had been destroyed by infarction before operation. Other causes or contributing causes of death were pulmonary embolism, myocardial infarction complicating angiography (ostial stenosis), and cerebral damage. Ten of the 14 vein grafts (71%) were patent at necropsy. A free flow of injection medium usually occurred between patent grafts and coronary arteries. Thrombosis of a graft was thought to have contributed to death in 3 patients, but not in a fourth who died of pulmonary embolism. Since thrombosis of grafts was usually secondary to poor run-off blood into severely atheromatous coronary arteries, this was also an indirect effect of the advanced coronary arterial disease. In one case, thrombosis followed severe chronic intimal thickening of a graft in place for 13 months. The study of these deaths emphasizes that in some patients the pathological changes in the coronary arteries and left ventricle are too severe for them to benefit from surgery. Vein grafts cannot be expected to distribute blood effectively through grossly narrowed coronary arteries. In addition, when a large part of the left ventricle is infarcted or scarred, it is almost certain that improving the blood supply by grafting will not result in significant regeneration of cardiac muscle. Since the time when this study was made, there have been few deaths among the many vein graft operations subsequently carried out in the hospitals involved. The two most important factors thought responsible for the improvement are the selection of cases more suitable for surgery by continued improvement of diagnostic techniques, and also the employment of more radical surgical procedures in the form of coronary endarterectomy and the insertion of more grafts per patient.     

Coronary arterial thrombosis and transmural myocardial infarct. Cause or consequence?]

Macroscopical examination at postmortem of 64 patients who died of their first transmural myocardial infarction (32 with anterior infarctions, 28 with posterior and 4 with lateral), during the first 30 days after the onset of symptoms, has shown that in 59 cases (92.2 p. 100) there was a totally occlusive thrombosis in the coronary artery. In all cases these thromboses were sited on the major coronary arterial trunk to zone of muscle which was destroyed, and on top of an ulcerated atheromatous plaque. The age of the thrombosis and the infarction were identical. There was no relationship between the presence (59 cases) or the absence (5 cases) of coronary arterial thrombosis with the age, sex, survival time or extent of the infarction. These postmortem findings are strongly suggestive of a fairly constant cause and effect relationship between coronary arterial thrombosis and acute transmural myocardial infarction.     

The clinical course, early prognosis and coronary anatomy of subendocardial infarction.

The following prospective study was undertaken to observe the clinical course, early prognosis and coronary anatomy of patients with subendocardial infarction. Subendocardial infarction was defined as typical chest apin (greater than 15 minutes), serum enzyme elevation and persistent (greater than 48 hours) new T wave inversion and/or S-T segment depression in the absence of new pathologic Q waves. Fifty consecutive patients were defined, followed in a prospective manner and subjected to early coronary arteriography. A prior history of unstable angina was found in 33 patients (66 per cent); 22 patients (44 per cent) had significant dysrhythmias during the acute hospital phase, and seven patients (14 per cent) had evidence of mild left ventricular failure. Coronary arteriography demonstrated significant lesions (greater than 75 per cent narrowing in at least one vessel) in all 50 patients, with 30 patients (60 per cent) having either double- or triple-vessel disease. Follow-up (mean 10.6 months) revealed that 15 patients (30 per cent) had stable angina, 23 patients (46 per cent) unstable angina and only 12 patients (24 per cent) remained free of angina. Of 28 patients in a medically treated group, acute transmural infarctions developed in six (21 per cent) and one died (3 per cent). We conclude that subendocardial infarction is symptomatically an unstable entity, is associated with severe coronary artery disease and, in a medically treated group, is followed by a significant incidence of early transmural myocardial infarction (21 per cent). Therefore, these patients require in-hospital monitoring, careful follow-up and consideration for early coronary arteriography.     

血栓栓塞导致急性心肌梗死的临床研究

目的探讨血栓栓塞导致急性心肌梗死的临床特点及预后。方法回顾性分析8例血栓脱落至冠状动脉致急性心肌梗死患者的临床资料,并进行随访。随访内容包括死亡、再次心肌梗死、严重出血、其余部位栓塞事件及国际标准化比值（INR）达标情况。结果患者年龄（63±15）岁。5例为风湿性心脏病换瓣术后患者,1例为肥厚型心肌病患者,2例为扩张型心肌病患者。患者心电图均表现为急性ST段抬高性心肌梗死,其中前壁心肌梗死6例,下壁心肌梗死2例。7例合并心房颤动（87.5%,7/8）。所有患者行急诊冠状动脉造影可见冠状动脉栓塞,其中5例行血栓抽吸术,3例行血栓抽吸及球囊扩张术。院内随访期间,发生大面积脑栓塞死亡1例,国际标准化比值达标率87.5%（6/7）,其余患者未再出现栓塞及严重出血事件。结论血栓栓塞导致心肌梗死发生于血栓形成高危人群,均表现为急性ST段抬高性心肌梗死,急性期使用血栓抽吸术尽早开通冠状动脉,术后予以规范的抗栓治疗,患者预后良好。     

Pathology of acute myocardial infarction with particular reference to occlusive coronary thrombi.

Analysis of the pathological findings in 500 cases of fatal acute myocardial infarction showed that in 469 this was localized to one transmural area of the left ventricle; in 31 there was diffuse subendocardial necrosis. In the former occlusive coronary thrombus was found in the related artery in 95 per cent of cases. Variation in the percentage of occlusions found was noted between different prosectors and when coronary artery calcification was present. Only 4 of the 31 patients with subendocardial necrosis had recent occlusion; triple vessel disease was common in this group suggesting general failure of coronary perfusion. It is essential in necropsy studies of the relation of coronary thrombosis to myocardial infarction to be sure that muscle necrosis is present, to distinguish the two forms of myocardial necrosis, and to employ a meticulous dissection technique with decalcification of the arteries when necessary.     

Ischemic myocardial injury during cardiopulmonary bypass surgery

ECG's and serum levels of SGOT, LDH, and CPK were examined during the immediate postoperative period in 126 patients who had cardiac surgery during cardiopulmonary bypass. None had coronary disease and valve replacement was performed in 97 patients. Miscellaneous procedures not involving the coronary arteries were performed in 29. In surviving patients, ECG signs of acute myocardial infarction appeared in 8 (7 per cent) and changes compatible with acute ischemic injury were seen in 38 (30 per cent). Elevation of SGOT exceeding 90 units occurred in 32 per cent of patients and LDH levels over 900 units occurred in 37 per cent. In patients with ECG evidence of postoperative infarction or ischemia, 70 per cent had abnormal SGOT levels and 70 per cent had abnormal LDH levels. In 40 patients with SGOT levels exceeding 90 units, 80 per cent had ECG evidence of acute infarction or ischemia. In 80 patients without ECG changes, only 10 per cent had SGOT levels exceeding 90 units. CPK levels correlated poorly with ECG evidence of ischemia or infarction. Patients who demonstrated ECG and serum enzyme evidence of ischemic injury or myocardial infarction had longer total perfusion times during surgery (P < 0.001) but no relationship to aortic cross clamp time was observed. ECG evidence of acute myocardial ischemia with elevation of serum enzymes is frequently observed following cardiopulmonary bypass surgery. Serial ECG's and measurements of postoperative serum enzymes provide useful information regarding myocardial injury and the effectiveness of bypass perfusion in protecting the myocardium during cardiopulmonary bypass sugery.     

Immediate or delayed angioplasty during the acute phase of myocardial infarction. Apropos of 118 cases

The results of immediate percutaneous transluminal coronary angioplasty (PTCA) (260 +/- 167 minutes after onset of pain and an average of 56 minutes after thrombolysis) and deferred PTCA (average 9.6 days, range 1 to 30 days after infarction) were compared in 118 consecutive patients with acute myocardial infarction. The overall primary success rate of PTCA was 82.2 per cent; it was higher in those patients undergoing deferred angioplasty (96% vs 78%; p less than 0.05). The primary success rate of immediate PTCA was related to the severity of the stenosis before dilatation: 75 per cent success in occluded compared to 84 per cent in suboccluded vessels (over 90% stenosis) and 100 per cent success in vessels with under 90 per cent stenosis. Eighty one per cent of failed angioplasties occurred in patients with occluded arteries, the majority being left anterior descending (LAD) arteries (71.4%). The incidence of restenosis was 13.4 per cent. This complication was diagnosed at coronary arteriography performed 40 days after PTCA in 1 case, 47 days after PTCA in another case and at the 6 month control in 11 cases. Reocclusion was observed in 21 patients (21.7% of immediate successes). The occlusion was diagnosed at the first control after an average of 8 days in 15 cases. The interval between the onset of pain and thrombolysis and dilatation was significantly longer in the group with reocclusion compared with patients without reocclusion (314 minutes vs 193 minutes for thrombolysis, p less than 0.01; and 356 minutes vs 204 minutes fort PTCA, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Septic cortical thrombophlebitis

Thrombosis of cortical veins has been postulated as an important cause of seizures and focal neurologic deficits in patients with bacterial meningitis. Diagnoses from autopsies, angiograms, and medical records at Massachusetts General Hospital, 1960-1984, were reviewed to identify patients with septic cortical thrombophlebitis. Only 10 confirmed cases of septic cortical vein thrombosis without sagittal sinus thrombosis were found. Meningitis was present in nine patients; Streptococcus pneumoniae was isolated from the blood or cerebrospinal fluid of five patients. Common clinical manifestations included fever, seizures, and focal neurologic signs. Half the patients survived, but three had persistent disabilities. Cortical vein thrombosis could be documented in only approximately 1% of 790 cases of bacterial meningitis. In 97 patients with meningitis who died and had autopsies, cortical thrombophlebitis was identified in 5%. In autopsied patients, other pathologic processes including arteritis, ventriculitis, cavernous sinus thrombosis, and cerebral infarctions were usually more prominent than venous thrombosis. Cortical thrombophlebitis does not appear to be the major cause of seizures or focal neurologic signs during bacterial meningitis.