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The records of 483 patients admitted to the emergency room because of syncope were reviewed. Thirty seven patients (7.7%) were found to suffer from transient ischemic attack- (TIA) related syncope. This group is the subject of this report. Of these patients, 28 (76%) were men (mean age 71 years). Seven patients reported previous syncopal episodes. Past history revealed a high rate of ischemic heart disease (70%) and hypertension (68%). Concurrent neurologic symptoms, which led to the diagnosis of TIA-related syncope, included mainly vertebrobasilar symptoms: vertigo (in 55% of the patients), ataxia (46%), parasthesia (41%). Two patients most probably were presenting bilateral carotid artery disease. Various diagnostic tests (including electroencephalography, computed tomography, sonography, and cerebral angiography) were used to exclude other causes of syncope. During follow-up (mean 14.5 months) four patients (11%) had an additional episode of TIA and in three of them syncope reappeared. One patient had a complete stroke. We conclude that TIA is a much more frequent explanation for syncope than has been previously argued. These patients tend to be elderly males with high incidence of ischemic heart disease and hypertension. The concurrent neurologic symptoms, leading to the diagnosis, represent mainly vertebrobasilar territory ischemia.

Signal-averaged electrocardiograms were obtained in 53 consecutive patients with a first acute myocardial infarction (AMI) who survived the first 10 days of hospitalization. The recording was performed twice, at Day 1 and at Day 10 of hospitalization, in patients without bundle-branch block and who did not receive antiarrhythmic therapy. Signal-averaged ECGs were obtained with an instrument which analyzes the presence of late potentials (LP) in each individual precordial lead. There were 41 men and 12 women, mean age of 67 years. On Day 1, three patients had L.P (5.6%). On Day 10, LP was recorded in 11 patients (21%). In only one patient was LP transient. Patients who developed LP by Day 10 (absent in Day 1) had statistically significant lower root mean square (rms) voltage and higher QRS duration than patients who did not develop LP on Day 10. In conclusion, in patients with a first AMI who survive the initial hospitalization period and are not in need of antiarrhythmic therapy have an incidence of LP of 21%. A predischarge recording is preferable since this will maximize the chances of detecting LP.

The purpose of this study was to determine the coronary angiographic correlations (specifically disease of the left anterior descending coronary artery) of reciprocal ST segment depression appearing during inferior acute myocardial infarction. Forty six patients (41 men and five women; mean age 56 years) were allocated into two groups based on the extent of precordial ST segment depression: widespread (V1-V6) ST depression v localised (V1-V4) ST depression. Patients with no reciprocal ST depression or patients with ST depression in V1-V4 but with ST elevation in V5 and V6 (inferolateral acute myocardial infarction) were excluded. All patients were catheterised during hospital admission for infarction. Twenty four of the 28 patients with ST depression in V1-V6 had significant lesions in the left anterior descending coronary artery whereas 16 of the 18 patients with ST depression in V1-V4 had insignificant or no lesions in the left anterior descending artery. The sensitivity, specificity, and positive and negative predictive values of widespread ST depression in predicting disease in the left anterior descending coronary artery were 92%, 80%, and 86% and 89% respectively. In patients with inferior acute myocardial infarction and precordial ST depression, the extent of ST depression is of clinical significance. Widespread (V1-V6) ST depression suggests disease of the left anterior descending coronary artery, whereas localised ST depression (V1-V4) indicates its absence.

A retrospective review of the records of 135 patients with proven or suspected endocarditis, seen between January 1970 and December 1987, is presented. Among the findings: (1) Mitral valve prolapse (MVP) as an underlying lesion was more common in the 1980s group of patients (22%) than in the 1970s group (6%, p less than 0.01); (2) no significant difference was found in the occurrence of pathogens between the 1970s and the 1980s groups of patients; (3) in most patients (17 of 19) with MVP, the organisms isolated were Streptococci viridans; (4) most patients (15 of 17) with MVP had undergone a dental procedure without prior antibiotic treatment in the two months prior to admission. Prophylactic antibiotic treatment is suggested in patients with MVP undergoing dental procedure, especially in a subset of patients with flail or redundant valve leaflet as 16 of our MVP patients (out of 17) had this pathology on echocardiogram.

Eleven patients, three with acute anterior myocardial infarction and eight with anterior ischemia, who developed transient right axis deviation with a left posterior hemiblock pattern during the acute phase of myocardial infarction or ischemia are described (study group). A correlation between their electrocardiographic pattern and the angiographic findings was made. The arteriographie findings were compared with those of a group of 24 patients with acute anterior myocardial infarction or ischemia without transient right axis deviation (control group).The main electrocardiographic characteristics of the right axis deviation pattern were: 1) an average shift of the mean frontal axis to the right of 42° (10° to 94°); 2) increased voltage of R waves in leads II, HI and aVF and appearance of small Q waves or decreased voltage of Q waves if previously present in the same leads; 3) decreased voltage of R waves and appearance of deep S waves in lead aVL; and 4) inverted T waves and isoelectric ST segments in leads II, III and aVF.Coronary angiography revealed that the study group had a higher incidence of significant right coronary artery obstruction and collateral circulation between the left coronary system and the posterior descending artery than did the control group (100 versus 25% and 73 versus 0%, respectively; p < 0.01). There were no differences between the groups regarding left anterior descending and circumflex artery disease. Transient right axis deviation during anterior myocardial infarction or ischemia represents different degrees of left posterior hemiblock, which is probably a consequence of decreased blood supply to the left posterior fascicle and is highly correlated with the presence of significant right coronary artery stenosis and collateral circulation between the right and left coronary systems.

Elevated serum lactic dehydrogenase (LDH) levels, 595 to 615 microns/ml (normal less than 225 microns/ml) with predominance of LDH isoenzymes 2 and 3 was the early and only sign of occult malignant lymphoma in three patients. In the first patient, overt lymphoma appeared clinically only 2 months after the finding of elevated serum LDH levels, whereas in the other two asymptomatic patients, pathologic LDH levels were the only clues to the need for further diagnostic investigation. It is concluded that LDH may have a diagnostic value in the preclinical stage of malignant lymphoma. Thus, a patient with no apparent cause for elevated serum LDH levels warrants a thorough work-up including abdominal CT scan and even explorative laparotomy.

A total of 1744 patients admitted to the ICCU with acute myocardial infarction (AMI) were studied in 1462 consecutive days (1982-1986). The aim of the study was to check whether the localization of the AMI was time related. Anterior (anterolateral) (AW) (n = 834) versus inferior-posterior (inferolateral) (IPW) (n = 823) AMI were compared: a third group with isolated lateral wall (LW) AMI (n = 87) was included in the study. Significant differences between monthly AMI localizations were registered, but no rhythmicity (monthly, seasonal) was found. A small absolute prevalence of AW localizations was found in all four seasons, but monthly differences made those differences not statistically significant. Some significant correlation (p less than 0.01) was found between AW AMI domination and daily geomagnetic activity (GMA level I-IV). Only on days with low (quiet) levels of GMA were there more IPW AMIs. Adverse relationship was seen with LW AMI, relatively benign in AMI, was adversely correlated with GMA level (p less than 0.01). Differences in AW/IPW and left/right coronary artery autonomic receptors distribution and flow regulation and/or changes in cardiovascular homeostasis/coagulation, aggregation, viscosity, microcirculation, and so on connected with AMI expansion may be involved in these differences of AMI localization.

The effect of sublingual nifedipine 10 mg (pierced capsule) and isosorbide dinitrate (ISDN) 5 mg on plasma viscosity (Pl.V) was investigated in 60 consecutive patients 7-10 days after hospitalization for acute myocardial infarction (AMI), who were randomized for either nifedipine (30 patients) or ISDN (30 patients). Pl.V, hematocrit (Htc), and erythrocyte sedimentation rate (ESR) were measured 20 minutes before and thereafter at 5, 10, and 30 min after drug administration while in the recumbent position. Blood pressure (BP) and heart rate (HR) were determined before each blood sample. In 18 patients (60%) Pl.V decreased by greater than 0.05 centipoise (Cp) after nifedipine (0.0953 +/- 0.033 Cp p less than 0.001 vs. initial values). After ISDN, Pl.V decreased by greater than 0.05 Cp (0.0933 +/- 0.036 Cp) in only 7 patients (23%). Systolic blood pressure (SBP) fell by 11.7 +/- 14.6 mmHg after nifedipine and by 16 +/- 14 mmHg after ISDN (nifedipine vs. ISDN = NS). Diastolic blood pressure (DBP) fell by 8 +/- 9.6 mmHg after ISDN and by 6.6 +/- 19.3 mmHg after nifedipine (nifedipine vs ISDN = NS). HR, ESR, and Htc did not change after drug administration. It is thus concluded from our study that nifedipine 10 mg sublingual has a significant Pl.V-lowering activity compared to sublingual ISDN 5 mg in patients with AMI.

Thirty cases in which transient left anterior hemiblock (LAHB) obscured the diagnosis of right bundle branch block (RBBB) appearing during the first days of an acute myocardial infarction (AMI) are presented. Twenty-eight of the patients with AMI had a clear septal wall involvement, while the remaining two had an anterolateral and lateral wall AMI, respectively. These intraventricular conduction defects developed 2-120 hours (mean 64.9 +/- 26 hours) after the acute event, and persisted for 24 hours to 7 days (mean 63.1 +/- 35 hours). The ECG was characterized by a pure LAHB with wide QRS complexes and the presence of RBBB was shown by recording high V1 and right-sided chest leads. The vectorcardiogram was also useful in several cases. The clinical course of this type of bifascicular block was transient and benign, with an in-hospital mortality of 6.7%. No patient developed trifascicular or complete atrioventricular block and, therefore, we conclude that prophylactic installation of a temporary pacemaker is not indicated in this type of bifascicular block. The possible role of extracellular potassium released during acute myocardial necrosis in the pathophysiological mechanism of these blocks is discussed.

Of 760 consecutive cases with anterior acute myocardial infarction (AMI), 55 developed acute bundle-branch block (BBB), fascicular block, or high-degree atrioventricular block during the hyperacute ECG stage of AMI. According to the direction of the ST segment during the acute ischemic episode, patients were divided into two groups. Group A consisted of 32 patients who developed BBB during ST-segment elevation, positive T wave, and absent or minimal Q wave. Group B consisted of 23 patients who developed BBB during ST-segment depression and evolved into anterior AMI. Group A was characterized by a higher incidence of right BBB and left anterior hemiblock [91% vs. 26% and 56% vs. 13%, respectively (p

Serum lactic dehydrogenase (LDH) isoenzymes were measured 24, 48, and 72 hours after administration in 85 patients with acute coronary insufficiency (ACI) and 10 patients with stable angina pectoris who served as controls. The above patients did not develop myocardial infarction according to the criteria of development of new Q waves or elevation of cardiac enzymes. In 15 patients with ACI a "flipped" LDH pattern (LDH1 greater than LDH2) was found in the presence of normal total LDH activity and normal creatine kinase-MB. The values of LDH 1:2 ratio ranged between 1.02 and 1.13 (normal values 0.45-0.75). In the 10 control patients, normal levels of total LDH and normal LDH enzyme distribution and creatine kinase-MB were found. A possible explanation for the flipped LDH pattern in the ACI patients (indicating some myocardial damage) could be myocytolysis and coagulation necrosis found on postmortem examinations. The conclusion of our study is that LDH isoenzymes should be measured in patients with ACI to determine the LDH 1:2 ratio. The finding of a "flipped" LDH pattern demonstrating myocardial damage, lacking in stable angina, may also be helpful in patients who developed the clinical picture of ACI more than 24 hours before arrival at the hospital, since by that time the creatine kinase-MB may have already returned to normal. An additional advantage of measuring LDH isoenzymes in these patients may be that patients with "flipped" LDH pattern may need a longer rest and earlier coronary angiographic evaluation.

Pacemaker carriers are at risk when undergoing operations involving the use of diathermy. The Shaw Scalpel utilizes a method by which the cutting edge of the blade is heated to a selected temperature that seals blood vessels as they are cut. No electrical currents are passed to or through the patient and there is no sparking or electrical arcing to the tissue. This apparatus was used as the sole method of thermal coagulation in 20 patients undergoing replacement of pacemaker batteries.

The records of 483 patients admitted to the emergency room because of syncope were reviewed. Forty-one patients were found to have drug-related syncope. Thirty-nine experienced syncope related to drugs administered for cardiovascular disease. The most frequently associated diseases were anginal syndrome (22 patients), hypertension (13 patients), and a history of myocardial infarction (6 patients). Thirty-eight patients experienced symptomatic orthostatic hypotension following drug taking (nitrates in 19 patients, beta blockers in 10 patients, nifedipine in 3 patients, prazosin and quinidine in 2 patients each, methyldopa and verapamil in 1 patient each). One patient developed complete heart block as a result of digoxin intoxication. Two patients developed the characteristic picture of anaphylactic reaction (1 with ampicillin, 1 with dipyrone). During one-year follow-up, without the offending medications, no further syncopal episodes were reported by these patients. We conclude that drug-related syncope was more common among our patients with syncope than had been reported previously. It is suggested that drug-related syncope should be taken into consideration in any patient with syncope who is treated by any of the above-mentioned drugs.

This study was undertaken in order to characterize the short-term (1 hour) and long-term (72 hours) effect of dobutamine on hemodynamic and regional ejection fraction parameters measured by radionuclear angiography in patients with chronic congestive heart failure due to coronary artery disease. Baseline hemodynamic and radionuclear parameters were measured and then intravenous dobutamine (8.5 mu/kg/min) was administered. The above parameters were determined again after 1 hour and 72 hours of continuous dobutamine administration. Sixty minutes (short-term) after dobutamine administration heart rate and cardiac index increased significantly (p less than 0.001 for both) and peripheral resistance decreased concomitantly (p less than 0.005). Global left ventricular ejection fraction (LVEF) as measured by multigated equilibrium nuclear angiography (MUGA) increased from 21.8 +/- 10.6% to 25 +/- 13.5 (p less than 0.02). Count-based mean regional ejection fraction in the septal, inferoapical, posterolateral (45 degrees left anterior oblique view) and inferior apical and anterolateral (30 degree right anterior oblique gated first pass) regions increased also. At 72 hours (long-term) after continuous dobutamine infusion, heart rate and cardiac index were still significantly higher and peripheral resistance lower than in the control study. However, global and count-based regional ejection fraction decreased to control values in the right anterior oblique view (first-pass analysis) and the left anterior oblique view (MUGA). Global LVEF measured in the right anterior oblique view by first-pass technique was significantly higher than control in the long-term study (23 +/- 9.7 vs. 27.8 +/- 2.4; p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

This study was designed to evaluate the effects of metaraminol (Aramine) in six patients with evolving acute inferior wall myocardial infarction accompanied by hypotension and warm limbs. There were 16 episodes of acute inferior wall ischemia, and the response to therapy was judged by evaluating blood pressure and ST segment and T wave abnormalities. Three patients received intravenous isosorbide dinitrate and two received streptokinase as the initial therapy. The mean ST segment elevation was significantly reduced (from 4.94 +/- 1 to 0.5 +/- 0.7 [p less than 0.0001]) after metaraminol infusion was initiated. The average T wave height also decreased (from 6.8 +/- 2 to -1.3 +/- 2.5 mm [p less than 0.0005]). The average heart rate decreased from 82 +/- 11 to 69 +/- 9 beats/min (p less than 0.05) and the mean arterial blood pressure increased from 81 +/- 12 mm Hg before metaraminol treatment to 126 +/- 8 mm Hg after treatment. All these changes occurred within a few minutes after metaraminol therapy was instituted. In 12 episodes, accelerated idioventricular rhythm appeared concomitantly with the resolution of ST segment elevation. Coronary angiography performed between 4 and 10 days after admission demonstrated significant obstruction in all infarct-related arteries, but none was totally occluded. Left ventricular function was normal in three patients and slightly hypokinetic in the inferior wall in two. These results indicate that in a selected group of patients with acute inferior myocardial infarction, metaraminol administration (in certain hemodynamic circumstances) can alleviate acute ischemia within a few minutes and thereby reduce ischemic injury.