Surgical treatment of myocardial infarction shock.
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Biomedical subjects
Publications and source records attributed to R R Miller.
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We compared cardiocirculatory actions of nitroprusside (NP) to prazosin (PZ) in eleven chronic coronary patients with refractory congestive heart failure. Each drug equally lowered systemic arterial pressures mildly while heart rate was unaltered. NP decline (P less than .001) in left ventricular filling pressure (28 to 17 mm Hg) and rise (P less than .005) in cardiac index (2.20 to 2.96 L/min/m2) were similar to PZ (30 to 17) and (2.08 to 3.00). PZ and NP equally enhanced cardiac efficiency of stroke work and myocardial oxygen consumption index. Total systemic vascular resistance declined (P less than .001) the same with NP and PZ. Forearm vascular resistance (FVR) and venous tone (FVT) diminished equally with NP and PZ. Similar FVR/FVT percent changes of 0.88 and 0.64 with NP and PZ indicated relatively balanced systemic arteriovenous relaxation. Sinze PZ effects persisted six hours with symptomatic improvement, oral PZ is the best vasodilator for long-term use, extending in-hospital NP-like actions to ambulatory heart failure therapy.
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The direct effects of 100, 300 and 500 mg/100 ml ethanol on contractility of isolated, supported right ventricular papillary muscles were evaluated from 10 normal or failing cat hearts. In isometrically contracting muscles, 500 mg% ethanol decreased maximum tension in normal and failing hearts from 7.1 to 4.3 g/mm2 (P less than 0.001) and 3.4 to 2.3 (P less than 0.01) respectively, and lowered maximum tension rise from 30.4 to 20.2 g/mm2/sec (P less than 0.001) and 10.2 to 0.8 (P less than 0.01), without alterations of time to peak tension. In isotonically contracting muscles, 500 mg% ethanol reduced contractile element velocity at 0.5 g/mm2 load in normal and failing ventricles from 1.27 to 0.97 L/sec (P less than 0.001) and 0.59 to 0.39 (P less than 0.001) respectively. Thus, clinically meaningful doses of ethanol clearly, exerted dose-related negative inotropic actions on both normal and failing myocardium, thereby indicating that ethanol ingestion may exacerbate heart failure in diseased hearts.
To elucidate the hemodynamic effects of prazosin, an antihypertensive agent, in congestive heart failure, we studied 10 patients with ischemic cardiomyopathy and severe ventricular dysfunction. After an oral dose of 2 to 7 mg, heart rate was unchanged (P greater than 0.05). One hour after prazosin administration, mean arterial pressure declined from 95 to 78 mm Hg (P less than 0.001); left ventricular filling pressure declined from 30 to 18 mm Hg (P less than 0.001), cardiac index increased from 2.1 to 2.9 liters per minutes per square meter (P less than 0.001), and systemic vascular resistance fell from 2074 to 1156 dynes sec cm-5 (P less than 0.001). In both forearms vascular resistance and venous tone were reduced (86 to 48 mm Hg per ml per 100 g per minute, and 59 to 18 mm Hg per ml, respectively [P less than 0.001]). All responses persisted for a least six hours (P less than 0.01). Prazosin benefits severe congestive heart failure by inducing a sustained fall of both cardiac preload and impedance.
We compared a coronary risk profile (developed by the Framingham Study) based on age, sex, cigarette smoking, glucose intolerance, left ventricular hypertrophy, systolic blood pressure and serum cholesterol to angiographically determined severity of coronary-artery disease in 158 consecutive patients undergoing cardiac catheterization. A profile of 1.0 indicated average relative risk. Risk profiles for 105 patients with angiographically documented coronary-artery disease was 1.52 whereas it was 1.08 for the group without coronary disease (P less than 0.01). There was no difference between the patients with coronary disease with (1.44) and those without previous infarct (1.46). The coronary risk profile, however, increased with increasing severity of coronary disease. The high-risk coronary patient can be identified by seven easily measured risk factors, and the extent of coronary-artery disease increases with the number and severity coronary risk factors.
To evaluate the efficacy of coronary bypass surgery in reduction of sudden death, the prognosis of 286 similar patients with multivessel coronary stenosis was studied prospectively and the results of medical therapy (Group I, 114 patients) were compared with those of surgical therapy (Group II, 172 patients) after cardiac catheterization and coronary arteriography. During 39 months' evaluation of both groups, mortality from congestive heart failure and noncardiac causes did not differ (Group I, 14 percent; Group II, 8 percent) (P greater than 0.05). Sudden was evaluated in the remaining 217 patients (Group I, 96; Group II, 121 patients) who were matched for age (Group I, 52 years; Group II, 51 years); duration of overt coronary disease (Group I, 3.8 years; Group II, 4.0 years); angina pectoris (Group I, 83 percent; Group II, 95 percent); prior myocardial infarction (Group I, 77 percent; Group II, 74 percent); and congestive heart failure (Group I, 30 percent; Group II, 23 percent) (all P greater than 0.05). In addition, the prevalence of coronary risk factors was the same (P greater than 0.05) in both groups (hypertension, cigarette smoking, diabetes mellitus, lipid abnormalities and family history of coronary disease). Importantly, arteriography and catheterization established a similar extent and location of major coronary arterial stenoses and of ventricular dysfunction; two vessel disease (Group I, 32 percent; Group II, 33 percent) and three vessel disease (Group I, 68 percent; Group II, 67 percent); left ventricular end-diastolic pressure (Group I, 13; Group II, 14 mm Hg);cardiac index (Group I, 2.85; Group II, 2.91 liters/min per m2); and coronary collateral vessels (Group I, 58 percent; Group II, 61 percent) (all P greater than 0.05). Fifty-six percent of patients in Group II had multiple bypass grafts and a late patency rate (average 21 months) of 87 percent of one or more grafts. During subsequent prospective evaluation of over 3 years, bypass surgery provided greater symptomatic benefit of improved functional capacity (Group I, 12 percent; Group II, 69 percent) (P less than 0.05) and complete anginal relief (Group I, 30 percent; Group II, 60 percent) (P less than 0.05). Moreover, bypass surgery was associated with marked reduction in sudden death (Group I, 24 percent; Group II, 6 percent) (P less than 0.05). Thus, in patients with multivessel coronary disease carefully matched for clinical factors, hemodynamics, atherogenic precursors and coronary pathoanatomy, effective aortocoronary bypass surgery appeared to prolong survival by decreasing the incidence of sudden death, possibly by a decrease of unexpected fatal arrhythmias.
Among 26,294 hospitalized patients monitored by the Boston Collaborative Drug Surveillance Program (BCDSP), 8,948 (34%) received at least one antibiotic, and none were diagnosed as having drug-induced colitis to in-hospital antibiotic exposure. Seven patients who had taken antibiotics as outpatients, however, were admitted with antibiotic-associated colitis. Six of these patients had taken lincomycin prior to the onset of symptoms; one had taken ampicillin. Six of the patients were hospitalized at a New Zealand hospital and one at a hospital in Canada. The five patients with lincomycin-associated colitis at the New Zealand hospital were admitted over an 11-month period. Severe colitis due to antibiotics has been a rare event in the BCDSP experience, especially in the United States.
The effects of oral prazosin on the peripheral circulation were evaluated in 10 subjects, including 7 patients with chronic congestive failure due to coronary heart disease. To achieve this purpose the actions of 30 to 50 micrograms/kg body weight prazosin were assessed on both the forearm arteriolar and venous beds simultaneously with the use of the limb plethysmographic technique. Prazosin produced marked decline of forearm venous tone (FVT) from 44.5 +/- 12.3 to 14.3 +/- 3.1 mm Hg/ml (p less than 0.01) concomitant with marked decrease in forearm vascular resistance (FVR) from 70.2 +/- 11.4 to 48.4 +/- 4.9 mm Hg/ml/100 gm/min (p less than 0.05) which persisted for at least 60 mins without change in heart rate. These findings, demonstrating that prazosin induces systemic venodilation and peripheral arteriolodilation, indicate potential benefits of the oral drug for relief of pulmonary congestion and elevations of cardiac output in patients with chronic congestive heart failure.
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Despite widespread use of treadmill stress in the detection of coronary disease, detailed information relating the important features of coronary pathoanatomy to the ischemic response noted on the electrocardiogram is lacking. Accordingly, 91 consecutive patients undergoing graded maximal exercise tests (MEXT) who were found to have clinical stenosis (larger than or equal to 75 per cent luminal narrowing) of at least one of the three major coronary arteries on coronary arteriography were evaluated. Positive MEXT was defined as larger than or equal to 0.1 mV horizontal or downsloping S-T segment depression larger than or equal to 0.08 second beyond J point. Over-all sensitivity of positive MEXT was 59 of 91 (65 per cent) patients; 11 of 26 (42 per cent) with single vessel stenosis, 20 of 30 (66 per cent) with two vessel disease and 28 of 35 (80 per cent) with three vessel disease. In patients with two vessel disease, the frequency (p less than 0.05) of positive MEXT was greater in those with (15 of 21;71 per cent) than in those without (five of nine; 55 per cent) stenosis of the left anterior descending artery. Concerning the site of intravessel stenosis, the frequency of positive MEXT was greater (p less than 0.05) with stenosis proximal to the left anterior descending artery in patients with one vessel disease. Quantification of total numbers of intra- and intervessel stenoses revealed 2.7 stenoses in the 59 patients with positive MEXT in contrast (p less than 0.01) to 1.9 in 32 patients with negative MEXT. Similarly, graded luminal narrowing index of severity of total stenoses per patient was 9.9 in those with positive MEXT compared (p less than 0.01) to 6.1 in those with negative MEXT. The poststenotic myocardial perfusion index, estimated by graded distal vessel opacification per major vessel disease, was only 1.5 in those with positive MEXT contrasted (p less than 0.01) to 2.4 in those with negative MEXT. These data indicate that sensitivity of positive MEXT in patients with coronary disease is most closely determined by the number of major coronary vessels involved, the total number of major vessels stenosed, the severity of total stenoses and poststenotic distal vessel perfusion. Less important factors are the precise site of intravessesl stenosis and the specific major coronary artery involved, although stenosis proximal to the left anterior descending artery favored positive MEXT. Unimportant variables were the quality of collateral vessels, ventricular function and prior inferior infarction. Angina occurred more frequently in those with positive MEXT, and marked degree of positive MEXT indicated stenosis proximal to the left anterior descending artery.
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Enhanced electrical stability of acutely ischemic myocardium with vagal stimulation and acetylcholinesterase inhibition has been demonstrated experimentally. To extend these findings clinically, within 24 hours of acute myocardial infarction, 11 patients underwent continuous 10 hour Holter monitoring: 2.5 hour control before and after 5 hour constant edrophonium infusion (0.25 to 2.00 mg./minute). Continuous infusion of the agent lowered heart rate 92 to 78 b.p.m. (p less than 0.01). Although mean total ventricular extrasystoles (PVC's) per 5 hours per patient (131) and PVC's per 1,000 beats (4.7) were unchanged (p greater than 0.05), potentially lethal tachyarrhythmias (malignant PVC's: multifocal, R on T, paried, greater than 5 per minute or ventricular tachycardia) were terminated in six of 10 patients by edrophonium. However, serious ventricular arrhythmias continued in three patients and appeared in four despite the agent. Ventricular fibrillation did not occur during the 10 hour period of study. In addition, the patients were evaluated hemodynamically and by His bundle electrograms before and after a 10 mg. bolus of edrophonium prior to the 10 hour constant infusion: heart rate declined (88 to 72 b.p.m., p less than 0.01), while mean arterial pressure (98 mm. Hg), left ventricular filling pressure (14 mm. Hg), cardiac index (2.4 L. per minute per square meter), and stroke work index (36 Gm.m./M.2) were unchanged (p greater than 0.05). The edrophonium bolus prolonged the A-H interval (117 to 135 msec., p less than 0.01) while the H-Q interval was unaltered (48 msec; p greater than 0.05). It is concluded that increased vagal tone with edrophonium did not reduce the over-all presence of premature ventricular contractions in the entire study group; however, the malignant nature of PVCs and ventricular tachycardia appeared to be lessened by the parasympathomimetic agent in certain patients. In addition, no adverse hemodynamic or intraventricular conduction effects were produced by edrophonium administration.
To evaluate the effectiveness of oral vasodilator therapy in chronic congestive heart failure, 20 mg of isosorbide dinitrate or placebo was administered orally in double-blind fashion to 25 patients with congestive heart failure. In 15 patients receiving isosorbide dinitrate, pulmonary arterial wedge pressure decreased 5 minutes to 5 hours after drug administration; the peak reduction was observed at 1 hour (from 23 to 14 mm Hg; P less than 0.001). Wedge pressure decreased to normal (12 mm Hg or less) in 8 of the 15 patients (Group I) but remained greater than 12 mm Hg in 7 (Group II). Reductions in mean systemic arterial pressure, systemic vascular resistance and pressure-time per minute also occurred. Indexes of pump output were unchanged in the 15 who received isosorbide dinitrate but tended to decrease slightly in Group I. Stroke index (from 23 to 26 cc/m2) and stroke work index (from 21.4 to 24.1 g-m/m2) increased slightly but significantly (P less than 0.05) in Group II. Thus the prinicpal hemodynamic action of isorbide dinitrate is marked and sustained reduction in left ventricular filling pressure without pronounced effect on cardiac output. This agent should be used in congestive heart failure primarily for relief of congestive symptoms.