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| Year : 1977 | Volume
: 23
| Issue : 1 | Page : 19-24 |
Serum free fatty acids and arrhythmias after acute myocardial infarction
VS Singh, S Kirti, TN Mehrotra, GP Elhence, RK Aran
Department of Medicine and Biochemistry, L. L. R. M. Medical College, Meerut (U.P.), India
Correspondence Address:
V S Singh
Department of Medicine and Biochemistry, L. L. R. M. Medical College, Meerut (U.P.)
India
 Source of Support: None, Conflict of Interest: None  | Check |
PMID: 615254 
Serum free fatty acid (FFA) levels measured in 72 patients with on acute myocardial infarction have been related to prevalence of arrhythmias, the clinical state of patients and to the serum enzyme levels. Maximum elevation of serum FFA occurred within eight hours in most patients after acute myocardial infarction. Those with a striking elevation (above 1200 mEq/L) had an increased prevalence of serious arrhythmias and disorder of conduction. There was no correlation between serum FFA and clinical state of patients, except for cardio genie shock nor between serum FFA and serum glutamic oxaloacetic transminase levels, nor between serum enzyme levels and the prevalence of arrhythmias.
How to cite this article:
Singh V S, Kirti S, Mehrotra T N, Elhence G P, Aran R K. Serum free fatty acids and arrhythmias after acute myocardial infarction. J Postgrad Med 1977;23:19-24 |
How to cite this URL:
Singh V S, Kirti S, Mehrotra T N, Elhence G P, Aran R K. Serum free fatty acids and arrhythmias after acute myocardial infarction. J Postgrad Med [serial online] 1977 [cited 2022 Jan 18];23:19-24. Available from: https://www.jpgmonline.com/text.asp?1977/23/1/19/42787 |
| :: Introduction | |  |
Serum concentrations of free fatty acids (FFA) have been shown to be raised in patients with acute myocardial infraction. [8] In other studies several authors have suggested a positive relationship between serum FFA and complicating arrhythmias and death after myocardial infarction. [9],[13],[14] They were of the opinion that high circulating FFA levels, were associated with intracellular lipid disturbances which could in turn provoke the arrhythmias. Various authors considered that the lipid changes were merely coincidental and elevation of serum FFA may be due to other metabolic events such as increased catecholamine secretions or starvation. [4],[15],[17]
The present study was undertaken to find out (i) whether there is any relationship between serum FFA levels and arrhythmias and death in patients with acute myocardial infarction and (ii) to correlate the relation between enzyme glutamic oxaloacetic transaminase (GOT) and serum FFA levels.
| :: Material and Methods | | |
The clinical material consisted of 72 patients in the age group of 37 to 67 years (mean 53 years) with acute myocardial infarction admitted to the intensive coronary care unit of LLRM. Medical College, Meerut. Patients with diabetes mellitus were excluded from the present study. Heparin, theophylline catecholamines, clofibrate, steroids or antihypertensive drugs which are known to influence serum levels of FFA, were avoided in these patients.
The diagnosis of myocardial infarction was based on clinical and electrographic evidence, using the criteria recommended by W.H.O., [20] with a significantly raised serum levels of Glutamic Oxaloacetic Transaminase (GOT). Blood samples for FFA and GOT estimations were taken within twenty-four hours of the onset of chest pain. Fasting specimens could not be obtained unless the patient had been admitted during the night. A second blood specimen was obtained in fasting state on the morning after admission. Usually three specimens were obtained from each patient and the first two were taken within twenty-four hours of the onset of the symptoms. ECG tracings were taken whenever arrhythmia was observed.
Serum FFA and the enzyme glutamic oxaloacetic transaminase were estimated colorimetrically by the methods Anstall and Trujillo [1] and Reitman and Frankel [16] respectively and their normal ranges were 450-675 µequ/L and 3-21 LU. respectively as standardized in this laboratory by observations upon 25 controls.
| :: Results | | |
[Figure 1] above shows serial changes in serum FFA levels after acute myocardial infarction in 47 patients and in all of these cases 3 or more specimens were obtained. Most of the specimens taken within the first twelve hours were not obtained in the fasting state. Specimens obtained twenty-four hours or more after the onset of symptoms were taken after overnight fast. The striking elevation of serum FFA levels eight hours after the onset of symptoms compared with the levels at twenty-four hours and forty-eight hours is obvious. But the degree to which serum FFA levels are truly elevated during the first eight hours is less certain since it has not been possible to make sufficient observations so soon after the onset.
For the presentation, serum FFA levels in 72 patients have been grouped in four categories of approximately equal numerical size and the highest level recorded was 22000 µequ/L. Distribution of cases according to age, sex and different complications of myocardial infarction in each serum FFA group are shown in [Table 1]. The only significant correlation between severity and serum FFA level was observed in the cases of cardiogenic shock. Presence of left ventricular failure or congestive heart failure was not always associated with a high FFA levels.
[Table 2] shows serum FFA levels in various major arrhythmias which followed acute myocardial infarction. The incidence of all arrhythmias is greater in patients with serum free fatty acid levels above 1200 µeq/L compared with lower levels. A significant relation between higher serum FFA levels and death has been also observed.
There was no correlation between. SGOT and serum FFA levels but the mortality rate was significantly higher in patients with SGOT levels greater than 120 I.U./litre.
| :: Discussion | | |
Serious arrhythmias and both early and late death were more common in cases of acute myocardial infarction where serum FFA levels were markedly raised. In the present study, 22 of the 72 patients had serum FFA levels more than 1200 µeq/L of which 20 patients (91%) had complicating arrhythmias, while 33 of the remaining 50 patients (66%) who did not have arrhythmias revealed serum FFA levels below 1200µEq/L. Number of deaths were more in patients with serum FFA levels more than 1200 µeq/L (31%) in comparision to those whose FFA levels were below 1200µeq/L(12%).These observations have been supported by various workers who reported that arrhythmias during acute myocardial infarction are due to a direct deleterious effect of free fatty acids on injured myocardium, [4],[6],[9],[10],[19] but as yet, it cannot be excluded that the lipid mobilization leading to raised serum FFA and the arrhythmias both are direct effects of the raised plasma. catecholamine levels. [12] In our study serum FFA levels and clinical state could not always be correlated except for cardiogenic shock which was more commonly seen in patients with higher serum FFA levels. Kurien and Oliver [8] suggested that myocardial hypoxia and severe pain could be responsible for this rise in serum FFA levels, which is brought about by release of noradrenaline from myocardium and post ganglionic sympathetic nerve-endings causing mobilization of free fatty acids from adipose tissue. The observation that the prevalence of serious arrhythmias correlated positively with the height of the serum FFA levels but not with serum enzyme levels also suggests that it is not the extent of myocardial infarction but possibly the metabolic disturbances resulting from hypoxia and sympathetic stimulation that may lead to serious arrhythmias and death.
In other studies the level of catecholamines in the urine have been shown to be raised in cases of acute myocardial infarction complicated by arrhythmias and/ or cardiogenic shock. [7] and plasma nor. adrenaline concentration was raised after myocardial infarction and related directly or indirectly to the development o serious arrhythmias. [11] It follows that both these latter studies support the theory that the rise in the plasma FFA concentration in cases with myocardial infarction could be secondary to catecholamine induced fatty acid mobilization from adipose tissue.
It is a well known fact that catechola mines can induce disorders of rhythm after myocardial infarction and increase myocardial oxygen consumption and that prolonged sympathetic stimulation may be harmful to the myocardium. [18] Increased catecholamine levels could therefore aggrevate hypoxia of the infarcted myocardium predisposing to arrhythmias and failure. Sympathetic stimulation and catecholamines increases the susceptibility of the ventricles to disorganized behaviour and the likelyhood of ectopic beats in the vulnerable period of the cardiac cycle. [2] Since increased sympathetic activity and catecholamine [3],[5] can cause mobilization of FFA from adipose tissue with elevation of circulating albumin-bound FFA, the correlation between arrhythmias and elevated serum FFA levels observed in this study may merely be an indirect indication of increased circulating catecholamines.[Table 3]
| :: References | | |
| 1. | Anstall, H. B. and Trujillo, T. M.: Determination of Free Fatty Acids in plasma by calorimetric procedure. An appraisal of the method and comparison with other technics. Clin. Chem., 11: 741-747, 1965.  |
| 2. | Daggett, W. H. and Wallace, A. G. : Mechanism and therapy of Cardiac arrhythmias. Edited by L. S. Derifus and W. Likoff, New York P 64, 1966. |
| 3. | Gordon, R. S. and Cherkas, A.: Unesterified fatty acid in human blood plasma, J. Clin. Invest., 35: 206-212, 1956. |
| 4. | Gupta, D. K., Young, R., Jewitt. D. E., Hartong. M. and Opie, L. H.: Increased plasma free fatty acid concentrations and their significance in patients with acute myocardial infarction. Lancet., 2: 12091213, 1969. |
| 5. | Havel, R. J.: Some influences of the sympathetic nervous system and insulin on mobilization of fat from adipose tissue: Studies of the turnover rates of free fatty acids and glycerol: Anal, of the New York Academy of Sciences., 131: 91-101. 1965. |
| 6. | Henderson. A. H.. Most. A. S, and Sornenblick, E. H.: Depression of contractility in rat heart muscle by free fatty acids during hypoxia. Lancet, 2: 825-826, 1969. |
| 7. | Jewitt, D. E., Mercer. C. J., Reid, D., Valori, C., Thomas, M. and Shillingford. J. P.: Free noradrenaline and adrenaline excretion in relation to the development of cardiac arrhythmias and heart failure in patients with acute myocardial infarction Lancet, 1: 635-641, 1969. |
| 8. | Kurien, V. A. and Oliver, M. F.: Serum free fatty acids after acute myocardial infarction and cerebral vascular occlusion Lancet, 2: 122-127, 1966. |
| 9. | Kurien, V. A. and Oliver, M. F.: Arrhythmogenic action of free fatty acids in myocardial hypoxia. Abstracts VI world congress of Cardiology. London p. 240, 1970. |
| 10. | Kurien, V. A., Yates, P. A. and Oliver, M. F.: Free fatty acids, heparin and arrhythmias during experimental myocardial infarction. Lancet, 2: 185-187, 1969. |
| 11. | McDonald, L., Baker, C . , Bray, C . , McDonald, A. and Restieaux, N.: Plasma Catecholamines after myocardial infarction, Lancet, 2: 1021-1023, 1969. |
| 12. | Nelson, P. G.: Free fatty acids and cardiac arrhythmias, Lancet, 1: 783, 1970. |
| 13. | Oliver, M. F. Kurien, V. A. and Greenword, T. W.: Relation between Serum free fatty acids and arrhythmias and death after acute myocardial infarction. Lancet, 1: 710-714, 1968. |
| 14. | Oliver, M. F.: Metabolic response during impending myocardial infarction clinical implication. Circulation 48: 491-494, 1971. |
| 15. | Opie, L. H., Norris. R. N., Thomos, M., Holland, A. J., Owen, P. and Van Norden. S.: Failure of high concentration free fatty acids to provoke arrhythmias in experimental myocardial infarction. Lancet 1: 818-822, 1971. |
| 16. | Reitman, S., and Frankel, S.: A colorimetric method for determination of serum glutamic oxaloacetic and glutamic pyruvic transaminase. Amer. J. Clin. Path. 28: 56-63, 1957. |
| 17. | Rutenberg, H. L., Pamintuan, J. C. and Soloft, L. A.: Serum free fatty acids and their relation to complications after acute myocardial infarction. Lancet, 2: 559-564, 1969. |
| 18. | Steinberg, D.: Synthesis and breakdown of triglycerides in adipose tissue. In fat as a tissue, p. 127. Ed. by K. Rodahl and B. Issekutz McGraw Hill, New York, 1964. |
| 19. | Taylor, S. H., Saxton, C., Majid, P. A., Dykes, J. R. W., Ghosh, P. and Sarkar, J. B.: Insulin secretion following myocardial infarction with particular respect to the pathogenesis of cardiogenic shock. Lancet, 2: 1373-1378, 1969. |
| 20. | World Health Organisation: Tech. Rep. Ser. 168: 25, 1959. |
[Figure 1]
[Table 1], [Table 2], [Table 3]
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