Intra aortic balloon pumping in myocardial infarction and unstable angina

From 1972 to 1979 intra aortic balloon pumping (IABP) was attempted in 181 patients; catheter insertion failed in 13 (8%). More complications occurred with prolonged treatment but all three lethal complications (2%) were related to catheter insertion. Seventy-six patients had clinical cardiogenic shock after myocardial infarction (CSMI). Haemodynamically, 23 were classified as preshock: 15 (66%) could be weaned, 12 (53%) survived over 3 months; whereas only 27/51 patients (51%) haemodynamically classified as shock could be weaned and 21 (40%) survived over 3 months. Of forty-two patients with refractory angina at rest, 41 had prompt relief of pain after IABP, and subsequently underwent coronary artery bypasss grafting (CABG). Perioperative infarction rate was 8% (4/41), perioperative mortality was 7% (3/41). Total infarction rate was 11% (5/42), and total mortality 7% (3/41). Pain relief was prompt in 14/17 patients (82%) with refractory angina after infarction. Pain persisted in three patients: all three sustained an infarction, one died. Two patients were excluded from surgery. Twelve patients underwent CABG; none died, none developed MI. In eight patients persistence of pain suggested a slowly evolving MI, IABP abolished pain in seven. Conclusion: IABP has demonstrated its efficacy both in pump failure and in refractory ischaemia. However, its use is not without risks

Ventricular free wall rupture : sudden, subacute, slow, sealed and stabilized varieties

Six cases of acute myocardial infarction with blood in the pericardial sac are described. In one case rapid death followed myocardial rupture leaving no time for the possibility of intervention. Of two other cases acute symptoms developing after myocardial rupture, one was operated on promptly and the other, whose condition improved on pericardiocentesis, after a delay of a few hours. Both are now long term survivors A fourth patient probably had two episodes of rupture which apparently sealed off. He underwent cardiac catheterization, but no epicardial leak was found. Subsequently at operation a sealed myocardial rupture was detected and sutured over. The fifth patient suffered a silent myocardial rupture. A false aneurysm was diagnosed four months later and he withstood successful surgery. In the sixth patient, the course was similar to that of case 1, namely rapid death with a clinical picture suggestive of tamponade. Postmortem examination showed a covert rupture with some evidence of attempts to plug the opening. The purpose of this report is to emphasize the varying course which myocardial rupture can take

Angina pectoris, one to 10 years after aortocoronary bypass surgery

The incidence of angina pectoris (AP) after bypass surgery was assessed in 1041 patients operated on consecutively between 1971 and 1980. Of the 977 survivors, 920 (94%) participated in the study with a followup time varying from 1 to 10 years (mean 3.5 years). Post-operative angina pectoris was present at 1 year in 277 patients (30%), at 3 years in 46%, at 8 years in 50%. The pain limited usual physical activities in 17.5%, 30% and 25%, respectively at these times. Nonetheless, 89% of the respondents felt improved by surgery. Factors without predictive value for late outcome were sex, number of pre-operative diseased vessels, and pre-operative ejection fraction. A correlation was found between post-operative AP and younger age at surgery in the males only (P less than 0.001); between AP and patency rate of the bypass graft (P less than 0.005) and with the status of the coronary arterial tree at three years post-operatively (P less than 0.001) in both sexes. The percentage of patients with recurrent AP increased with time after surgery up to 3 years, but remained stable thereafter. In conclusion, post-operative AP seems initially related to decreased functioning of the bypass graft, later to progression of coronary sclerosis in the native circulation