Prognostic significance of acute systolic hypertension after myocardial infarction.

The clinical behaviour and mean peak serum aspartate aminotransferase (SGOT) values of 106 patients admitted to a coronary care unit with acute myocardial infarction who displayed acute systolic hypertension were studied. Another 106 normotensive patients with acute myocardial infarction acted as controls. Neither group had established hypertension. The mortality rate, incidence of cardiac failure, major arrhythmias, and mean peak SGOT were significantly greater in the hypertensive group, within which the duration of hypertension was correlated with mean peak SGOT levels--through there was no definite relation between the height of systolic or diastolic pressure and SGOT. Transient systolic hypertension after acute myocardial infarction was therefore associated with a relatively poor prognosis, but our observations suggest that patients with a systolic blood pressure of at least 170 mm Hg might benefit from early hypotensive treatment.     

Alterations of antithrombin III after acute myocardial infarction

The antithrombin III (AT III) activity and the AT III concentration were investigated in 62 consecutive patients with acute myocardial infarction (AMI). To identify the reactant pattern of AT III in postaggressive situations, we also determined labile and acute phase proteins. Firstly, 29 patients were nourished orally and then 33 patients were fed by i.v. hyperalimentation (additional caloric intake of approximately 1,000 cal). AT III activities and concentrations as well as prealbumin and retinol-binding protein decreased concomittantly and significantly whereas haptoglobin, C-reactive protein and fibrinogen increased significantly after AMI. The changes cannot be interpreted as being alterations of the haematocrit. The alterations of AT III correlated significantly with the changes of labile proteins but not with the acute phase reactant proteins. The AT III decrease in the postinfarctional phase may promote a prethrombotic state. In In addition it can be concluded from our results that AT III reacts as (nutritive-dependent) labile protein, which is lowered in postaggressive situation and does not increase as an acute phase reactant. This is in accordance with results from recent animal experiments.     

Prostate specific antigen levels after acute myocardial infarction

Prostate Specific Antigen (PSA), a member of kallikrein family, is a specific serine protease of prostatic tissue. In some case reports, changes in PSA levels after acute myocardial infarction (AMI) have been reported. In this study we evaluated variations in PSA levels post-AMI. Twenty-six male patients who had PSA levels within reference limits were included in the study. The diagnosis of AMI was confirmed by clinical findings, ECG (electrocardiogram) and cardiac marker studies. Serum total PSA (tPSA) and free PSA (fPSA) levels were measured at days 0 (day of admission), 1, 2 and 3 after AMI. PSA/albumin ratio was also calculated in order to evaluate the effect of dilution. A statistical analysis of the results of all patients revealed significant decrease in tPSA levels and tPSA/Albumin ratio at day 2 when compared to days 0 and 3, which showed a similar pattern. Changes of fPSA and fPSA/ Albumin ratio according to days were not found significant. In only four patients we found increased levels of tPSA and increased fPSA levels in three of them. These patients displayed severe problems such as renal failure, cardiac failure, ventricular aneurysm and cerebral ischemia due to cardiac arrest. The lower tPSA levels on day 2 suggest that tPSA can be eliminated rapidly from the circulation on days 1 and 2, probably through the formation of complexes of tPSA with acute phase proteins.     

Depression after myocardial infarction.

The Minnesota Multiphasic Personality Inventory was completed by 101 patients 16 to 18 months after a proved myocardial infarction. The data suggested a bimodal distribution of patients. One class of patients had a relatively "normal" personality score apart from a tendency to hypomania. The second class had severe depression, with associated hysteria, hypochondriasis and psychasthenia. The severely depressed patients were older, with a greater tendency to hypertension and angina, and a tendency to smaller gains in aerobic power despite an equal intensity of endurance training. The distinction between "normal" and "depressed" postinfarction patients seems of some clinical importance, for the two classes of patients require opposite supportive techniques--restraint and encouragement, respectively.