Significance and treatment of nocturnal angina preceding myocardial infarction

Significance and treatment of nocturnal angina preceding myocardial infarction

Significance and treatment of nocturnal angina preceding myocardial infarction Edgar Lichstein, M.D.* Carlos Alosilla, M.D. Kul D. Chadda, M.D.* Prem ...

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Significance and treatment of nocturnal angina preceding myocardial infarction Edgar Lichstein, M.D.* Carlos Alosilla, M.D. Kul D. Chadda, M.D.* Prem K. Gupta, M.D.* New York, N. Y.

Angina which disturbs sleep is termed nocturnal angina and may be the presenting manifestation of coronary heart disease. 1 Previous discussions of this entity have suggested different mechanisms which include association with dreaming, 2-4 decreased blood pressure, ~ and early congestive heart failure. ~. 5 In this study we compare various characteristics of patients with and without n o c t u r n a l angina and discuss its probable etiology. These characteristics include location of infarction, prior congestive heart failure, and cardiomegaly. Method

A total of 174 consecutive patients with acute myocardial infarction (MI) were evaluated in o u r coronary-care unit. The diagnosis of acute transmural MI was based on the presence of a history of typical precordial pain, the development of significant Q waves, and the typical evolution of serum enzymes. Anterior wall MI included both anteroseptal and anterolateral; inferior wall MI included inferoposterior and inferolateral MI. Those patients with a typical history and serial enzyme elevations consistent with acute MI but without the evolution of significant Q waves were diagnosed as having subendocardial infarction. At the time of admission, a questionnaire was From the Department of Medicine, Division of Cardiology, Mount Sinai Hospital Services, City Hospital Center at Elmhurst, Mount Sinai School of Medicine of the City University of New York, New York, N. Y. Received for publication April 1, 1976. Reprint requestsi Edgar Lichstein, M.D., Division of Cardiology, Maimonides Medical Center, 4802 Tenth Ave., Brooklyn, N. Y. 11219. *Present address: Division of Cardiology, Maimonides Medical Center, 4802 Tenth Ave., Brooklyn, N. Y. 11219.

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completed concerning the characteristics of the patient's pain and the patient's symptoms within the month prior to admission. This evaluation included questions concerning angina on exertion, nocturnal angina, and clinical symptoms of congestive heart failure. Nocturnal angina was defined as anginal pain which aroused a patient from sleep and was usually similar to the daytime chest pain. A history of clinical congestive heart failure was defined as dyspnea on exertion, orthopnea, or paroxysmal nocturnal dyspnea in the absence of any apparent noncardiac cause. Cardiomegaly was evaluated radiographically at the time of admission and was judged to be present if the cardiothoracic ratio was greater than 0.50. P values were obtained by chi-square statistical analysis. Results

Of the 164 patients studied, 104 (63%) had angina during the m o n t h prior to myocardial infarction. This included 23 (13 per cent) patients who experienced nocturnal angina. T he incidence of nocturnal angina was significantly higher in those with anterior MI (p < 0.005) and subendocardial infarction (p < 0.02) than in patients with inferior MI (Fig. 1). The group with nocturnal angina was comprised of 16 men and seven women with an average r~ge of 58 years; the group without nocturnal angina was comprised of 89 male and 43 female patients with an average age of 61 years. Congestive heart failure in the m o n t h prior to admission was more common in those with nocturnal angina (9/23) than in those without (3/141) (p < 0.001). Cardiomegaly was seen in

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L i e h s t e i n et al.

D

GO

NOCTURNAL ANGINA WITHOUT NOCTURNAL ANGINA

50 U) I.Z 40 bJ I,-

9/23 patients with nocturnal angina and 22/141 without (p < 0.02). Previous myocardial infarction as determined both clinically and electrocardiographically was seen in 10/23 patients with nocturnal angina (43 per cent) and 25/141 (18 per cent) of those without. The significant characteristics of those with and without nocturnal angina are listed in Table I and are shown graphically in Fig. 2. Discussion

20

ANTERIOR M.I,

INFERIOR M.I.

SUGI[NDOCARDIALM.L

Fig. 1. Incidenceof nocturnal angina in patients with anterior,

inferior, and subendocardial M.I. 50

NOCTURNAL ANGINA WITHOUT NOCTURNAL ANGINA

40 o

i

o/~ 3 0 "

20-

I0

-

CARDIOMEGALY

PRIOR C,H.R

PREVIOUS M.I.

Fig. 2. Incidenceof prior CHF, cardiomegaly,and previousMI in those with and without nocturnal angina. Table I. MI and nocturnal angina No.

Prior CHF

Cardio, megaly

Previous MI

9 0 0

4 0 6

11 9 2

10 9 6

Patients with nocturnal angina:

Anterior MI Inferior MI Subendocardial MI

15 2 6

4 0 5

Patients without nocturnal angina:

Anterior MI Inferior MI Subendocardial MI

724

56 63 22

2 1 0

The three possible mechanisms of nocturnal angina listed by Gorlin 1 include (1) a sympathetic discharge related to dreaming, (2) a decrease in blood pressure at night leading to inadequate perfusion of the m y o c a r d i u m , and (3) early congestive heart failure. Nowlin and associates 2 and others 3"4 described the association of nocturnal angina with dreaming. These studies monitored rapid eye movements (REM) during sleep to identify periods of dreaming. During these RE M periods, tachycardia and then ST-segment depressions were noted, suggesting t hat the dreaming process was the initiating cause. ST-segment elevation was noted during R E M sleep in one patient with variant angina. 6 Although most of the episodes o f nocturnal angina and ST-segment changes were associated with R E M periods, occasional episodes were seen during the stage of deep (Stage 4) sleep. ~ Possible explanations of the association of nocturnal angina and dreaming include a state of "physiologic arousal" which leads to an increase in systolic blood pressure, heart rate, and respiratory rate ~ and a general sympathetic discharge causing alterations in the coronary circulation2 Nowlin and associates 2 also suggested t hat an increased respiratory rate seen s h o r t l y after the onset of R E M activity could lower arterial carbon dioxide partial pressure, which could lead to decreased coronary artery diameter. T he association with dreaming could not be determined in our study since we felt t h a t information gathered at the time of admission would not be valid. The autonomic nervous system shows a redistribution of activity during quiet sleep with a general enhancement of parasympathetic over sympathetic activity.' Blood pressure falls, largely due to diminished peripheral resistance and heart rate decreases. T h e possibility t h a t nocturnal angina occurring during periods of quiet sleep

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Nocturnal angina preceding M I

could be due to decreased perfusion beyond a stenosed coronary artery cannot be excluded. Comparisons of anterior and inferior transmural MI have shown a higher mortality rate 8 and more left ventricular dysfunction in those with anterior wall involvement reflecting more extensive myocardial damage. 9 This is explained by the coronary artery a n a t o m y and its relationship to location of infarction. Although some variation exists, a greater proportion of the left ventricle is usually infarcted with occlusion of the left anterior descending coronary artery 9 and significant disease of this vessel has been found in 96 per cent of patients with anterior myocardial infarction? ~ Disease of the right coronary artery, which was noted in 87 per cent 9 of those with inferior MI, may lead to less my.ocardial necrosis. Hamb y and associates 1~ noted t hat a history of congestive heart failure and cardiomegaly was more common in patients with anterior MI than in patients with a normal QRS or inferior MI. T h e y also noted t h a t the group with multiple infarctions had abnormal hemodynamics, which would explain the occurrence of nocturnal angina in six of our patients with subendocardial infarction, all of whom had previous infarctions. We believe t h a t the increased myocardial oxygen demand associated with decreased ventricular function and ventricular dilatation is the most likely cause of nocturnal angina. This is based on our observation t ha t nocturnal angina was much more common preceding anterior MI farction a n d was associated frequently with congestive heart failure prior to admission and cardiomegaiy. It is of interest to note t ha t three of the four patients with nocturnal angina associated with dreaming reported by Nowlin and associates 2 were studied and all found to have significant two- or three-vessel disease. Their case No. 3 progressed to congestive heart failure requiring digitalis after the nocturnal angina subsided. With this probable mechanism in mind the treatment of nocturnal angina may differ from that of effort angina. Digitalis has been found to improve ventricular function and not aggravate symptoms in patients with uncomplicated angina ~2 and is suggested in the t r e a t m e n t of nocturnal angina. 5 Propranolol, which has been mentioned in the t r e a t m e n t of nocturnal

American Heart Journal

angina, 13 should be used with great care and probably in combination with digitalis. This combined therapy has been recommended TM in patients with large hearts in order to prevent further increase in heart size by propranolol. We conclude t hat the presence of nocturnal angina in those who develop MI increases the likelihood t h a t the infarction will be either anterior or subendocardial rather t han inferior. T h e association of nocturnal angina and congestive heart failure to anterior MI is probably due to more severe and probably significant left coronary artery disease in patients having nocturnal angina. In addition to routine t r e a t m e n t of heart failure with salt restriction, diuretics, and digitalis, propranolol should be used with caution and consideration given to early coronary angiography. Bypass surgery may prove beneficial in those patients with good ventricular function. Summary The presence of nocturnal angina and congestive heart failure within the m o n t h prior to admission was evaluated in the 174 patients with acute myocardial infarction. H eart size was evaluated radiographically at the time of admission. Twenty-three patients (13 per cent) experienced nocturnal angina. T h e incidence of nocturnal angina was significantly higher in those with anterior myocardial infarction (p < 0.005) and subendocardial infarction (p < 0.02) when compared with patients with inferior MI. Congestive heart failure was more common prior to admission in those with nocturnal angina (9/23) as opposed to those without (3/141) (p < 0.001). Cardiomegaly was seen in 9/23 patients with nocturnal angina and 22/141 without (p < 0.02). We conclude t hat the presence of nocturnal angina in those who develop MI increases the likelihood t h a t the infarction will be either anterior or subendoeardial rather t han inferior. T h e association of nocturnal angina and congestive heart failure to anterior myocardial infarction is probably due to more severe and probably significant left coronary artery disease. We thank Mr. Manuel Beekermanfor the art workand Mrs. Edith Eriek for secretarial work. REFERENCES 1. Gorlin,R.: Pathophysiologyof cardiac pain, Circulation 32:138, 1965.

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2. Nowlin, J. B., Troyer, W. G., Collins, W. S., Silverman, G., Nicholas, C. R.; McIntosh, H. D., Estes, E. H., Jr., and Bogdonoff, M. D.: The association of nocturnal angina pectoris with dreaming, Ann. Intern. Med. 63:1040, 1965. 3. Editorial: Nocturnal angina, Lancet 1:732, 1972. 4. Sleight, P.: Nocturnal angina. Letter to the Editor, Lancet 1:903, 1972. 5. Hurst, J. W.: The heart, ed. 3, New York, 1974, McGrawHill Book Company, Inc., p. 1021. 6. King, M. J., Zir, L. M., Kaltman, A. J., and Fox, A. C.: Variant angina associated with angiographically demonstrated coronary artery spasm and R E M sleep, Am. J. Med. Sci. 265:419, 1973. 7. Bristow, J. D., Honour, A. J., Pickering, T. G., and Sleight, P.: Cardiovascular and respiratory changes during sleep in normal and hypertensive subjects, Cardiovasc. Res. 3:476, 1969. 8. Norris, R. M., Brandt, P. W. T., Caughey, D. E., Lee, A. J., and Scott, P. J.: A new coronary prognostic index, Lancet 1:274, 1969. 9. Russell, R. O., Jr., Hunt, D., and Rackley, C. E.: Left

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10.

11.

12.

13. 14.

ventricular hemodynamics in anterior and inferior myocardial infarction, Am. J. Cardiol. 32:8, 1973. Williams, R. A., Cohn, P. F., Vokonas, P. S., Young, E., Herman, M. V.~ and Gorlin, R.: Electrocardiographic, arteriographic and ventriculographic correlations in transmural myocardial infarction, Am. J. Cardiol. 31:595, 1973. Hamby, R. I., Hoffman, I., Hilsenrath, J., Aintablian, A., Shanes, S., and Padmanabhan, V.: Clinical hemodynamic and angiographic aspects of inferior and anterior myocardial infarctions in patients with angina pectoris, Am. J. Cardiol. 34:513, 1974. Sharma, B., Majid, P. A., Meeran, M. K., Whitaker, W., and Taylor, S. H.: Clinical, electrocardiographic and haemodynamic effects of digitalis (ouabain) in angina pectoris, Br. Heart J: 34:631, 1972. Besterman, E.: Nocturnal angina. Letter to the Editor, Lancet 1:1067, 1972. Crawford, M. H., LeWinter, M. M., O'Rourke, R. A., Karliner, J. S., and Ross, J. Jr.: Combined propranolol and digoxin therapy in angina pectoris, Ann. Intern. Med. 83:449, 1975.

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