Effects of alternate routes of epinephrine delivery in experimental bradycardia-hypotension.

The magnitude and rapidity of response to epinephrine given by various routes were evaluated using a new model of bradycardia and hypotension. In ten animals, left ventricular (LV) injection of 10 micrograms/kg of epinephrine was superior to right ventricular (RV) injection in regard to time to attain a 20% increase in heart rate (HR), a 10% increase in mean arterial pressure (MAP) and time to reach peak MAP, although the peak MAP itself did not significantly differ. Similar results occurred with a 15 micrograms/kg dose. Aortic injection in seven of the animals resulted in a much longer time to target HR, an equal time to target MAP and a longer time to peak MAP compared to LV injection. LV injection of epinephrine results in a significantly more rapid onset of action than RV injection in the bradycardic, hypotensive animal. Epinephrine's beneficial effect appears to be derived from its vasoconstrictive, chronotropic and inotropic properties.

Two-dimensional echocardiography versus surface electrocardiography for the diagnosis of acute non-Q wave myocardial infarction.

The initial two-dimensional echocardiogram (2DE) and electrocardiogram (ECG) of 50 consecutive patients with chest pain and a possible acute non-Q wave myocardial infarction (MI) were compared to each other to determine the value of 2DE in this type of acute MI. The ECG markers for a non-Q wave MI were (1) greater than or equal to 0.15 mV ST segment depression, (2) ST segment elevations with reciprocal ST segment depression, and (3) new symmetrical deep T wave changes as compared to a recent preadmission ECG. The 2DE was considered positive for MI if akinesia, dyskinesia, or severe hypokinesia was seen in one or more left ventricular segments. The sensitivity, specificity, and predictive value of the 2DE as compared to the ECG was 66% and 52%, respectively (sensitivity); 91% and 95%, respectivity (specificity); and 91% and 94%, respectively (predictive value). Statistically, there were no differences in the proportion of patients who had a positive 2DE as compared to the proportion of patients who had a positive ECG (p greater than 0.2). The ECG and 2DE results were combined and the sensitivity increased to 76% but the specificity decreased to 86%. Myocardial infarction size was not significantly different in infarcted subjects who had a positive 2DE (395 +/- 125 IU/L) as compared to those who had a negative 2DE (727 +/- 187 IU/L, p greater than 0.1).

Non-transmural infarction: clinical distinction between patients with ST depression and those with T wave inversion.

The electrocardiograms and clinical characteristics of 152 patients with chest pain, who had changes only in their ST or T waves, were evaluated. The increase in ST depression was significantly greater (p less than 0.01) in infarction patients than in those without infarction; this was not the case with T wave inversion (p greater than 0.5). Infarction patients with ST depression had a higher incidence of previous myocardial infarction and prior digitalis usage (74% versus 35%, p less than 0.01) and a significantly greater short term (37% versus 12%, p less than 0.05) and long term (52% versus 19%, p less than 0.02) mortality than infarction patients who had T wave inversion alone. This difference was unrelated to infarct size as determined by peak enzyme levels. These two groups, therefore, appear to be clinically distinct, perhaps related to differences in ventricular function and/or extent of coronary artery disease.

Persistent ST-segment elevation and left ventricular wall abnormalities: a 2-dimensional echocardiographic study.

Twenty-three patients with an anterior wall myocardial infarction (MI) and persistent ST-segment elevations (Group I) were examined for wall motion abnormalities using 2-dimensional (2-D) echocardiography. Twenty-two (96%) had dyskinetic wall motion of the infarcted area and 10 (43%) had a left ventricular aneurysm. Among 15 patients who had a chronic anterior wall MI without ST-segment elevation (Group II), 13 (86%) had akinesia of the infarcted segment. To document that dyskinetic wall motion caused the persistent electrocardiographic ST-segment elevations, 15 patients with an acute anterior wall MI (Group III) were followed by serial 2-D echocardiography for 2 to 24 months (mean 8). Of the 10 patients who had dyskinetic wall motion abnormalities on their initial 2-D echocardiogram, persistent ST-segment elevation developed in 9. All 5 patients with akinetic or severely hypokinetic wall motion abnormalities on their first 2-D echocardiogram did not show ST-segment elevation on late follow-up surface electrocardiograms. Infarct size as determined by peak creatine kinase levels for the former subgroup was greater than that for the latter subgroup (2243 +/- 429 vs 899 +/- 320 IU, respectively, p less than 0.01). In conclusion, persistent ST-segment elevation after an acute anterior wall MI is indicative of dyskinetic wall motion rather than aneurysm formation. Dyskinesia precedes the appearance of ST-segment elevation and is probably responsible for these changes on the surface electrocardiogram. Infarct size is larger in persons in whom dyskinetic wall motion abnormalities are likely to develop.

Coronary artery spasm occurring late after vein graft surgery.

A patient with classic effort and high-grade, fixed proximal coronary atherosclerosis underwent a single saphenous vein graft to a large, dominant right coronary artery (RCA). After being asymptomatic for 1 1/2 years, she had several episodes of rest angina culminating in Prinzmetal angina and ventricular fibrillation. Electrocardiographic changes occurred in the RCA distribution. Symptoms subsided with oral nifedipine therapy. Angiography revealed intact vein graft and coronary circulation. The patient has done well for a follow-up period of 7 months.

Alternating Wenckebach periods with acute myocardial infarction. Report of two cases.

This report describes two patients with the spontaneous occurrence of alternating Wenckebach periods during the course of acute myocardial infarction. Both patients demonstrated alternating Wenckebach periods which terminated in a sequence of two blocked P waves. In one patient, His bundle electrocardiographic study documented the site of block to be proximal to the His bundle. Alternating Wenckebach periods with the block proximal to the His bundle may be compatible with a benign prognosis.

Lactic dehydrogenase isoenzyme determination in the diagnosis of acute myocardial infarction.

Lactic dehydrogenase (LD) isoenzymes were determined by a rapid, simple technique and their utility in the diagnosis of acute myocardial infarction (AMI) was evaluated. LD isoenzymes were separated by ion-exchange column chromatography using DEAE-Sephadex. The cardiac fractions (LD-1 and LD-2) were measured separately on an Abbott ABA-100 analyzer and ratio of LD isoenzyme 1 to LD isoenzyme 2 (LD1:2) calculated. Daily serum samples were obtained from 100 patients selected only for a history of chest pain of abrupt onset. In 47 patients whose diagnosis was acute myocardial infarction (AMI), confirmed by typical clinical presentation and typical rise in cardiac-specific creatine kinase isoenzyme (MB(, peak LD1:2 ranged from 0.77 to 2.26. In 44 patients without AMI, peak LD1:2 ranged from 0.25 to 0.76. In two patients with electrocardiographic changes chest pain occurred two and five days previously; there was no rise in MB, but LD1:2 was elevated. Four patients with small AMI had no rise in LD1:2. Three more patients (one with active hemolysis) had false positive results. Thus, there was a sensitivity of 96% and a specificity of 97% when the cut-off point was LD1:2 = 0.76. LD1:2 is not quite as sensitive or specific as MD, but the ratio allows for the diagnosis of infarction in cases where MB has already returned to normal.

Detection of cardiac-specific creatine kinase isoenzyme in sera with normal or slightly increased total creatine kinase activity.

We describe a spectrophotometric kinetic assay for detecting creatine kinase MB isoenzyme activity in the 1 to 10 U/liter range. The MB isoenzyme was isolated [Clin. Chem. 20, 36 (1974)] and assayed (Rosalki method) with an Abbott ABA-100. Good reproducibility was demonstrated for MB isoenzyme activities near 1 U/liter (CV = 2.6%). Sera with normal or slightly increased total creatine kinase activity were evaluated. Sera of 14 patients with acute myocardial infarction contained, per liter, 84 to 236 U of total creatine kinase activity and 4.6 to 28.0 U of isoenzyme MB activity; corresponding ranges for sera from healthy lab technicians and patients with noncardiac disease were 36 to 277 and 0 to 2.6 U. MB isoenzyme activity for infarction patients rose and fell sharply within three days after the infarction. Atypical time-course patterns, MB isoenzyme activity remaining abnormally great for five days, were observed in serum from patients with prolonged atrial fibrillation and congestive heart failure or cardiomyopathy; the BB isoenzyme (1 to 5 U/liter) was also detected in sera of such patients but was absent in sera from infarcation patients. Quantification of column-isolated MB by the assay described is rapid, easy, specific, and extremely sensitive for measuring MB in the 1 to 10 U/liter range.

Cardiac specific creatine phosphokinase isoenzyme in the diagnosis of acute myocardial infarction.

The specific and sensitivity of serum creatine phosphokinase cardiac specific isoenzyme (MB) in the diagnosis of acute myocardial infarction (AMI) was evaluated. An ion-exchange chromatographic technique was used to isolate MB. Sera layered on mini-columns of DEAE-Sephadex were eluted with Tris-buffered sodium chloride. Quantification of isolated MB was performed by creatine phosphokinase (CPK) assay (Rosalki method) of column effluents. MB was expressed as a percentage of the simultaneously determined total serum CPK; MB was determined in 100 consecutive admissions to the Coronary Care Unit. Acute myocardial infarction was diagnosed by accepted criteria. In 47 patients with proven AMI, including three with normal total CPK, peak MB was greater than 4% of total CPK. In 49 patients without AMI, including 15 with elevated total CPK (due to trauma, injections, cardioversion), peak MB was less than 2% of total CPK. MB was elevated, but did not peak in four patients without AMI but with chronic atrial fibrillation. Isolation and quantification of MB by this technique is rapidly and easily performed and provides a specific and extremely sensitive tool for the diagnosis of AMI.