In ambulant outpatients with chronic HF, low serum sodium and SDNN and high serum creatinine identify patients at increased risk of death due to progressive HF.

SUMMARYInfarct size was assessed quantitatively in 33 patients with acute myocardial infarction with a new technic based on analysis of serial serum creatine phosphokinase (CPK) changes to determine its relationship to prognosis. We have recently measured infarct size in the conscious dog with this method which takes into account CPK distribution space, fractional disappearance rate, proportion degraded in myocardium, and proportion released into the circulation, and we have validated the method by measurement of myocardial CPK depletion in the same animals. In the present study, CPK activity (determined spectrophotometrically) and isoenzyme profiles (assayed electrophoretically) were measured in patient serum samples obtained every 2 hours. Infarct size was estimated by mathematical analysis of serial CPK changes utilizing the method previously developed in the conscious dog model. CPK isoenzyme profiles demonstrated prominent anodal bands, absent from normal serum, indicating that enzyme elevations reflected CPK released from heart rather than skeletal muscle. In 19 class I-II survivors (New York Heart Association) estimated infarct size was 31 + 4 CPK-gram-equivalents (CPK-g-Eq). It was significantly larger (P < 0.01), 103 +-14, in nine patients who died and in four class III or IV survivors (91 8). Estimation of cumulative infarct size differentiated patients with electrocardiographic changes and clinical sequelae from complications such as pericarditis from those patients with extension of infarction. Thus, infarct size can be assessed quantitatively in patients with acute myocardial infarction and provide a useful diagnostic and prognostic index based on the extent of myocardial damage.

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The effects of glucose-insulin-potassium (GIK) infusion and glucose (G) infusion started 30 min after experimental coronary occlusion and the combination of GIK and propranolol (P) started 3 hours after coronary occlusion on the development of myocardial infarction were studied in 37 dogs. Fifteen minutes after the coronary occlusion, epicardial electrocardiograms were recorded at 10-15 sites; 24 hours later transmural specimens were obtained from the same sites for determination of myocardial creatine phosphokinase (CPK) activity and the evaluation of morphologic changes. In the control group (normal saline infusion) the relationship between S-T-segment elevation (mv) 15 min after occlusion and CPK activity (IU/mg of protein) 24 hours later was: log CPK = -0.064 S-T + 1.24; r = 0.81. In the GIK group, the infusion was begun 15 min following epicardial mapping, and sites with the same S-T-segment elevations showed less CPK depression than did the control group: log CPK =-0.022 S-T + 1.25. The G group also showed less CPK depletion than the control group but to a somewhat lesser extent than the GIK group (log CPK = -0.030 S-T + 1.20). The group receiving GIK and P 3 hours after occlusion also showed less CPK depression than did the control group (log CPK =-0.034 S-T + 1.26). Histologic analysis in 24-hour specimens showed that sites which exhibited S-T-segment elevation 15 min after occlusion showed normal histology in 3% of specimens obtained from control dogs, while the other 97% showed early signs of myocardial infarction. However, in the GIK group, 36% of the specimens with S-T-segment elevation prior to the infusion were histologically normal 24 hours later, while in the G group 30% were normal, and in the GIK and P group 17% were normal. Electron microscopy confirmed the morphologic changes observed by light microscopy. Thus, in the presence of experimental coronary occlusion, GIK exerts a protective effect against myocardial ischemia and reduces the extent of myocardial necrosis. G alone acts similarly but to a lesser degree, while a beneficial effect can also be demonstrated when GIK and P are started 3 hours after the onset of coronary occlusion.

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SUMMARY We investigated the effects of brief intermittent periods of ischemia on myocardial viability. Brief periodic coronary occlusions were produced up to 18 times by inflating and deflating the balloon of an intracoronary #2F catheter for periods of 15, 10 or 5 minutes, followed by 15-minute periods of reperfusion. Creatine kinase (CK) release, triphenyl tetrazolium chloride staining, and light and electron microscopy were used to detect the presence of myocardial necrosis. For the study of CK release, blood was taken from the great cardiac vein and the aorta before and at 5-minute intervals during each left anterior descending coronary occlusion, as well as during and 1, 5, 10 and 15 minutes after balloon deflation. In seven of 24 dogs with 15-minute occlusions, in five of 21 dogs with 10-minute occlusions, and in three of 32 dogs with 5-minute occlusions, small but distinct areas of subendocardial necrosis were present. In all dogs with morphologic proof of necrosis, there was periodic release of CK into the great cardiac vein, which peaked immediately after reperfusion, reflecting CK washout. Thus, brief periods of ischenia, which when single do not cause necrosis, have a cumulative effect and may cause myocardial necrosis. This mechanism of necrosis may be relevant clinically in patients with frequent anginal episodes. Since many dogs of this study did not have any myocardial necrosis, the findings also suggest that intermittent repefdusion has a beneficial effect and may prevent necrosis, even when total occlusion time exceeds 200 minutes.EXPERIMENTAL STUDIES have established that to cause myocardial necrosis, an ischemic injury must be of sufficient duration and severity. Even with the severest ischemia in dogs, the injury must be present for at least 20-30 minutes before necrosis will occur.1 For example, if flow is restored after 15 minutes of ischemia, no myocardial necrosis will be present. ' However, even when ischemia is brief and myocardial necrosis does not occur, there is usually a lengthy delay in return of normal function and metabolism in the injured myocardium.2-Therefore, we evaluated the possibility that brief periods of ischemia before the myocardium has fully recovered from the effects of preceding episodes of ischemia may gradually increase the degree of injury to the point of nonreversibility and necrosis. Methods PreparationThe study was with room air was instituted with a Harvard respirator. Systemic blood pressure was measured through a catheter inserted into the femoral artery. A #5F catheter was inserted through the external jugular vein under fluoroscopic control into the coronary sinus and advanced into the great cardiac vein. The position was verified by injection of contrast material. A #7F Judkins catheter was inserted through the left carotid artery into the ostium of the left anterior descending coronary artery (LAD). A #2F Fogarty catheter was then passed through the lumen of the Judkins catheter and advanced 2-3 cm into the LAD. The Judkins catheter was withdrawn into...

Background: The authors of prior small studies raised the hypothesis that symptoms in veterans of the 1991 Gulf War, such as chronic diarrhea, dizziness, fatigue, and sexual dysfunction, are due to cholinergic autonomic dysfunction. Objective: To perform a confirmatory test of this prestated hypothesis in a larger, representative sample of Gulf War veterans.

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