icum. Cas. Lik. (es., 98, 529. (1963). Prispevek vysetrovani fibrinolysis.Lab. Vise- trovani (Prague), 9, 816. ... Sang, 29, 62. Rub, D., Fekete, T., and Ionescu, ...
Brit. Heart J., 1969, 31, 447.
Serum Cholinesterase and Euglobulin Lysis Time in Chronic Cor Pulmonale ST. HARAGU$, M. CUCUIANU, AND P. MISSITS From I Medicale Clinic Cluj, Cluj, str. Clinicilor nr. 3, Rumania Frank myocardial infarction is very seldom enSUBJECTS AND METHODS countered in patients with chronic cor pulmonale. In a preliminary study (Haragus et al., 1966) serum Among the 179 patients with myocardial infarction cholinesterase was investigated in patients with chronic admitted to our clinic between 1956 and 1965 there cor pulmonale and heart failure: 28 patients with corowere none with chronic cor pulmonale. However, nary heart disease with congestive heart failure, and 32 anatomo-pathological data show that atherosclerotic patients with rheumatic valvular disease and right-sided changes in the aorta are not less frequent in sub- heart failure. Serum cholinesterase, serum cholesterol, plasma jects with cor pulmonale than in control subjects fibrinogen, fibrinolytic activity were subsequently of the same age (Rub, Fekete, and Ionescu, 1967). investigated and in the following groups of patients. In addition, among 303 patients with decompenGroup A included 30 healthy young subjects without sated chronic cor pulmonale admitted to our clinic first-degree relatives affected by atherosclerosis. over a period of five years, there were none with a Group B was composed of 30 atherosclerotic patients peripheral thrombophlebitis. However, this does (14 men, 16 women) between 52 and 78 years, without not exclude the occurrence of thromboembolic heart failure, most of them survivors of myocardial episodes in the pulmonary vessels of patients with infarction. chronic cor pulmonale. Indeed it has been sugGroup C included 17 patients (12 men, 5 women) gested that thrombosis of pulmonary vessels could between 25 and 68 years (mean 54 years) with chronic be a cause of the cor pulmonale (Dexter, 1965). cor pulmonale and heart failure, selected according to Changes in platelets and coagulability in cor pul- W.H.O. criteria (1961), namely: (a) presence of a monale have been previously reported (Beltrami chronic disease of lungs likely to produce chronic cor pulmonale; (b) signs of hypertension in the pulmonary and Bucher, 1966; Bouvier and Koralnik, 1962; arteries; (c) right ventricular hypertrophy. All these Donner, 1959). We therefore decided to investi- patients had hepatic enlargement. The jugular venous gate plasma fibrinogen and fibrinolytic activity in pressure was not measured. This group contained this disorder. only "pure " cases of chronic cor pulmonale without An impairment in the production of serum pro- coronary heart disease. It should be remembered teins and lipoproteins, including factors involved that congestive heart failure in a patient with chronic in coagulation and fibrinolysis, is to be expected disease of the lungs is not always due to pulmonary in chronic cor pulmonale, when the liver is affected disease, and could be due to associated atherosclerotic by congestive heart failure. Estimation of the coronary artery disease, though frank myocardial inhepatic involvement in this condition is a difficult farction is uncommon. Therefore, a further group was studied, Group D, task, since liver function tests in cardiac patients 14 patients (10 men, 4 women) between 42 containing are influenced by extrahepatic factors. It has been 80 years (mean 57 years) with decompensated found, however, that serum cholinesterase is a and chronic cor pulmonale, complicated by coronary heart reliable indicator of the proteosynthetic function disease or generalized atherosclerosis, and presenting one of the liver (Hall and Lukas, 1937; Antopol, or several of the following characteristics: first degree Schifrin, and Tuchman, 1938; Cucuianu, Mure§an, relatives affected by coronary heart disease; arterial and Mure§an, 1966), and is not directly influenced hypertension; diabetes mellitus; atrial fibrillation or by extrahepatic factors or haemodynamic changes angina pectoris on exertion. The presence of coronary heart disease in these cases could be strongly inferred. (Hlrigu§ et al., 1966). Received October 16, 1968.
Nine patients were found to have enlargement of the liver. 447
H4ar4argus, 448
Cucuianu, and Missits TABLE
SERUM CHOLINESTERASE, SERUM CHOLESTEROL, PLASMA FIBRINOGEN, EUGLOBULIN LYSIS TIME, AND THE RATIO PLASMA FIBRINOGEN/EUGLOBULIN LYSIS TIME IN YOUNG HEALTHY CONTROLS (A), ATHEROSCLEROTIC PATIENTS WITHOUT HEART FAILURE (B), AND PATIENTS WITH HEART FAILURE DUE TO "PURE" COR PULMONALE (C) OR CHRONIC COR PULMONALE COMPLICATED BY CHRONIC ISCHAEMIC HEART DISEASE (D) _ _ _ _ _ _
_
_
_
_~~~~
_
~
~
_
-T~~~
A
Group
_
B
_
_
_
20
30
17
17
Mean SE
227 ±9
280 ±14
139 ±17
168 ±20
Serum cholesterol (mg./100 ml.)
Mean SE
163* ±4
230 ±8
165 ±6
197 ±12
Plasma fibrinogen (mg.1100 ml.)
Mean
283
503
533
731
SE
±12
±31
±46
±73
Mean
285
612
SE
±17
±28
185 ±22
460 ±65
Mean SE
1 0-06
0-8 ±005
No. of observations
Serum cholinesterase (,umole/ml. per hr.)
Euglobulin lysis time (min.)
Plasma fibrinogen/euglobulin lysis time
* It should be mentioned here that mean values of serum cholesterol than those generally reported in Anglo-Saxon or Scandinavian reports.
1-9
4 ±0-6
were
found
±0 4
to
_
_
_
_
Statistical significance (p)
D
C
A vs B < 0-01
A vs C < 0-001 A vs D < 0-001 B vs C < 0-001 B vs D < 0-001 C vs D>0-1
A vs B < 0 001 A vs C>0-1 A vs D < 0 05 B vs C
