Research Journal of Pharmacology and Pharmacodynamics

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Depression: As a Risk Factor for Coronary Heart Disease


Affiliations
1 Department of Pharmacology, P.S.G.V.P.M’s College of Pharmacy, Shahada. Department of Pharmacology, Ahinsa Institute of Pharmacy, Dondaicha, India
     

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We conducted a review to resolve whether there is relationship between depression and coronary heart disease or not. Depression is a mental health problem which is spread widely and most of physicians are well acquainted with this concept of depression. Diagnosis of depression disorder based on continuity of illness, etiology of illness and number of symptoms - all these discriminations should be reported during inspecting the link between depression and coronary heart disease. We review the mechanism of linking depression and coronary heart disease i.e. relationship between depression and inflammation, depression and autonomic dysfunction, CHD and autonomic dysfunction, depression and Sleep architecture disruption, depression and circadian rhythm disruption, CHD and circadian rhythm disruption, and depression and behavioral mechanism. There is bidirectional association between depression and coronary artery disease i.e. coronary artery disease can cause major depressive disorder and depression is risk factor for CAD and its complications. Major depression is a devastating comorbid disease that can make recovery difficult and increase risk of cardiac mortality and morbidity. We also go over the therapy options like Psychotherapy, Electroconvulsive therapy, Exercise etc. But there are some antidepressant medications also available for treating depression in patients associated with CAD. The antidepressant medications like SSRIs e.g. Sertraline, fluoxetine, citalopram etc. appears to be safe in individual with depression and concomitant CAD or unstable angina. However, some evidence suggests that SSRIs like tricyclics, may increase risk cardiac events and death when taken for long time. New classes of antidepressants have dual reuptake inhibition for serotonin and nor-epinephrine e.g. venlafaxine. These medications are slightly more successful than SSRIs in treating depression, but they also have some adverse effects. Selegiline transdermal form was recently licensed for the treatment of MDD. Oral selegiline is not effective antidepressant. When compared to oral selegiline, STS results in stable plasma levels of drug and increased drug concentration in the brain.

Keywords

Coronary heart disease, Depression, CAD, Venlafaxine.
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  • Cassem H, Hackett TP, psychiatric consultation in coronary care unit, Ann Intern Med 1971(75),9-14.

  • Cay EL, Vetter N, Philip AE, Dugard P, psychological status during recovery from acute heart attack, J Psychosom Res 1972(16), 425-435.

  • Croog SH, Levine S, life after Heart Attack, New York Human sciences press Inc., 1982.

  • S. Moussavi, S. Chatterji, E.Verdes, A. Tardon, V. Patel, and B. Ustun, “Depression chronic disease and decrements in healthhealth; results from world Health surveys,” Lancet 2007 (370), no. 9590, pp. 851-858,

  • Lichtman JH, Froelicher ES, Blumenthal JA, carney RM, Doering LV, Frasuresmith N, Freedland KE, Jaffe AS, Leifheit - Limson EC, sheps DS, Vaccarino V, Wulsin L, American Heart Association Statistics Committee Of Council On Epidemiology and prevention and council on cardiovascular and Stroke Nursing Depression as risk factor for poor prognosis among patients with acute coronary syndrome: systematic review and recommendations,a scientific statement from American Heart Association circulation 2014 (129),1350-1369.

  • Vaccarino V. Bremner JD, Behavioral, emotional and neurobiological determinants of coronary heart disease risk in women, Neurosci Blobehav Rev 2017 (74), 297-309.

  • D. Lloyd-Jones, R.J. Adams, T.M. Brown et al, “Heart disease and stroke statistics-2010 update,a report from American Heart Association”, Circulation 2010 (121), no.7, pp. e46-e215.

  • R.M. Carney and K.E. Freedland, “Depression in patients with coronary heart disease”, American Journal of Medicine 2008 (121), no. 11, Supplement, pp. S20-S27.

  • D.E. Bush, R.C. ziegelstein, U.V. Patel et al, “post myocardial infarction depression”, Evidence Report / Technology Assessment 2005,no. 123, pp. 1-8.

  • J.P. Van Melle, P. De Jonge, T. A. Spijkerman et al, “prognostic association of depression following myocardial infarction with mortality and cardiovascular events, a meta-analysis,” Psychosomatic Medicine 2004 (66), no.6, PP. 814-822.

  • N.Frasure- Smith and F. Lesperance, “Reflection on depression as a cardiac risk factor”, Psychosomatic Medicine 2005 (67), Supplement 1, PP.S19-S25, 2005.

  • American Psychiatric Association, Diagnostic and Statistical Manual of Mental Disorders, 5th ed. Arlington, VA: American Psychiatric Association; 2013.

  • Penninx BW, Depression and cardiovascular disease, epidemiological evidence on their linking mechanisms, Neurosci Biobehav Rev 2017 (74), 277-286.

  • W.M.MCDonald, I. H. Richard, and M.R.Delong, “prevalence, etiology and treatment of depression in Parkinson’s disease,” Biological Psychiatry 2003 (54), no.3, pp.363-375.

  • H. A Pincus, W. W. Davis, and L.E.Mcqueen, “subthreshold” mental disorders, a review and synthesis of studies on minor depression and other “brand names” British Journal of Psychiatry 1999 (174), pp. 288-296.

  • 16 W.E. Broadhead, D. G. Blazer, L.K. George, and C.K. Tse, “Depression disability days, and days lost from work in prospective epidemiologic survey,” Journal of American Medical Association Association 1990 (264),no. 19, pp. 2524-2528.

  • I. B. Hickie, G. Andrews, and T. A. Davenport, “Measuring outcomes in patients with depression or anxiety: an essential part of clinical practice,” Medical Journal of Australia 2002 (177), no. 4, pp. 205-207.

  • M.E. Maruish, “Handbook of psychological assessment in primary care settings," in Handbook of psychological assessment in primary care settings, Lawrence Erlbaum 2000 Mahwah, NJ, USA.

  • Mason JC, Libby P, Cardiovascular disease in patients with chronic inflammation: mechanisms underlying premature cardiovascular events in rheumatologic conditions. Eur Heart J 2015; 36:482-9c.

  • L. M. Biasucci, “CDC/AHA workshop on markers of inflammation and cardiovascular disease: application to clinical and public health practice: clinical use of inflammatory markers in a patients with cardiovascular diseases: a background paper,” Circulation 2004 (110),no. 25, pp. e560-567.

  • N. H. Wallen, C. Held, N. Rehnqvist, and P. Hjemdahl, “Elevated serum intercellular adhesion molecule-1 and vascular adhesion molecule-1 among patients with stable angina pectoris who suffer cardiovascular death or non-fatal myocardial infarction,” European Heart Journal 1999 (20), no. 14, pp. 1039-1043.

  • N. T. Mulvihill, J. B. Foley, R. T. Murphy, R. Curtin, P. A. Crean, and M. Walsh, "Risk stratification in unstable angina and non-Q wave myocardial infarction using soluble cell adhesion molecules,” Heart. 2001 (85), no. 6, pp. 623-627.

  • P. M. Ridker, C. H. Hennekens, J. E. Buring, and N. Rifai, “Creactive protein and other markers of inflammation in the prediction of cardiovascular disease in women,” New England Journal of Medicine. 2000 (342), no. 12, pp. 836-843.

  • R. M. Carney, K. E. Freedland, R. C. Veith et al., “Major depression, heart rate, and plasma norepinephrine in patients with coronary heart disease,” Biological Psychiatry 1999 (45), no. 4, pp. 458-463.

  • H. W. Koenigsberg, M. H. Teicher, V. Mitropoulou et al., “ 24 h Monitoring of plasma norepinephrine, MHPG, cortisol, growth hormone and prolactin in depression,” Journal of Psychiatric Research 2004 (38), no. 5, pp. 503-511.

  • R.C. Veith, N. Lewis, O.A. Linares et al., “Sympathetic nervous system activity in major depression: basal and desipramineinduced alterations in plasma norepinephrine kinetics,” Archives of General Psychiatry 1994 (51), no.5, PP. 411-422.

  • P. W. Gold, M. L. Wong, D. S. Goldstein et al., “Cardiac implications of increased arterial entry and reversible 24-h central and peripheral norepinephrine levels in melancholia,” Proceedings of the National Academy of Sciences of the United States of America. 2005 (102), no. 23, pp. 8303-8308.

  • P. J. Schwartz, “The autonomic nervous system and sudden death,” European Heart Journal. 1998(19), pp. F72-F80.

  • N. P. Andrews, D. S. Goldstein, and A. A. Quyyumi, “Effect of systemic alpha-2 adrenergic blockade on the morning increase in platelet aggregation in normal subjects,” American Journal of Cardiology.1999 (84) no. 3, pp. 316-320.

  • R. M. Benca, W.H obermeyer, R.A. Thisted, J.C.Gillin, D.J.Kupfer, and C.F. Reynolds, “sleep and psychiatric disorders: a meta-analysis,” Archives of General Psychiatry. 1992 (49), no.8, PP. 651-670.

  • U. John, C. Meyer, H.J. Rumpf, and U. Hapke, “ Relationships of psychiatric disorders with sleep duration in an adult general population sample,” Journal of Psychiatric Research. 2005 (39), no. 6, pp. 577-583.

  • C.F.Reynolds and D. J. Kupfer, “sleep research in affective illness: state of the art circa 1987,”sleep 1987 (10), no.3, pp.199-215.

  • D.J. Kupfer and M.E. Thase, “The use of the sleep laboratory in diagnosis of affective disorders,” Psychiatric Clinics of North America. 1983 (6), no.1, PP. 3-25.

  • J. shen, S. A. Chung, L. Kayumov et al., “polysomnographic and symptomatological analysis of major depressive disorder patients treated with mirtazapine,” Canadian Journal of Psychiatry. 2006 (51), no. 1, PP. 27-34.

  • D. Kunz and W. M. Herrmann, “Sleep-wake cycle, sleep-related disturbances, and sleep disorders: a chronobiological approach,” Comprehensive Psychiatry 2000 (41), no. 2, Supplement 1, pp. 104-115.

  • D. H. Avery, S. H. Shah, D. N. Eder, and G. Wildschiedtz, “nocturnal sweating and temperature in depression,” Acta Psychiatrica Scandinavica. 1999 (100), no. 4, pp. 295-301.

  • D. H. Avery, G. Wildshiodtz, and O. J. Rafaelsen, “Nocturnal temperature in affective disorder,” Journal of Affective Disorders. 1982 (4), no. 1, pp. 61-71.

  • W. C. Duncan Jr., “Circadian rhythms and the pharmacology of affective illness,” Pharmacology and Therapeutics. 1996 (71), no. 3, pp. 253-312.

  • E. Souetre, E. Salvati, J. L Belugou et al., “Circadian rhythms in depression and recovery: evidence for blunted amplitude as the main chronobiological abnormality,” Psychiatry Research. 1989 (28), no. 3, pp. 263-278.

  • E. Souetre, E. Salvati, T. A. Wehr, D. A. Sack, B. Krebs, and G. Darcourt, “Twenty-four-hour profiles of body temperature and plasma TSH in bipolar patients during depression and during remission and in normal control subjects,” American Journal of Psychiatry. 1998 (145), no. 9, pp. 1133-1137.

  • M. P. Szuba, B. H. Guze, and L. R. Baxter, “Electroconvulsive therapy increases circadian amplitude and lowers core body temperature in depressed subjects,” Biological Psychiatry. 1997 (42), no. 12, pp. 1130-1137.

  • L. Wetterbuerg, J. Beck-Friis, B. Aperia, and U. Petterson, “Melatonin/cortisol ratio in depression,” Lancet. 1979 (2), no. 8156-8157, article 1361.

  • J. Arendt, A. Wirz-Justice, J. Bradtke, and M. Kornemark, “Longterm studies on immunoreactive human melatonin,” Annals of Clinical Biochemistry. 1979 (16), no. 6, pp. 307-312.

  • J. Mendlewicz, P. Linkowski, L. Branchey, U. Weinberg, E. D. Weitzman, and M. Branchey, “Abnormal 24 hour pattern of melatonin secretion in depression,” Lancet. 1979 (2), no. 8156- 8157, article 1362.

  • M. C. Cohen, K. M. Rohtla, C. E. Lavery, J. E. Muller, and M. A. Mittleman, “Meta-analysis of the morning excess of acute myocardial infarction and sudden cardiac death,” American Journal of Cardiology. 1997 (79), no. 11, pp. 1512-1516.

  • J. E. Muller, P. H. Stone, and Z. G. Turi, “Circadian variation in the frequency of onset of acute myocardial infarction,” New England Journal of Medicine. 1985 (313), no. 21, pp. 1315-1322.

  • R.M. carney, K.E. freedland and A.S. Jaffe, “Altered circadian pattern of acute myocardial infarction in patients with depression,” Coronary Artery Disease. 1991 (2), no. 1, pp. 61-65.

  • P. M. Ho, J. A. Spertus, F. A. Masoudi et al., “Impact of medication therapy discontinuation on mortality after myocardial infarction,” Archives of Internal Medicine. 2006 (166), no. 17, pp. 1842-1847.

  • J. N. Rasmussen, A. Chong, and D. A. Alter, “Relationship between adherence to evidence-based pharmacotherapy and longterm mortality after acute myocardial infarction,” Journal of the American Medical Association. 2007 (297), no. 2, pp. 177-186.

  • I. M. Kronish, N. Rieckmann, E. A. Halm et al., “Persistent depression affects adherence to secondary prevention behaviors after acute coronary syndromes,” Journal of General Internal Medicine. 2006 (21), no. 11, pp. 1178-1183

  • B. K. Nallamothu, K. A. A. Fox, B. M. Kennelly et al., “Relationship of treatment delays and mortality in patients undergoing fibrinolysis and primary percutaneous coronary intervention. The Global Registry of Acute Coronary Events,” Heart. 2007 (93), no. 12, pp. 1552-1555.

  • Spijkerman TA, van den Brink RH, Jansen JH, et al. Who is at risk of post-MI depressive symptoms? J Psychosom Res. 2005 (58), 425-432.

  • Pratt LA, Ford DE, crum RM, et al. Depression, psychotropic medication, and risk of myocardial infarction: Prospective data from the Baltimore ECA follow-up. Circulation. 1996 (94), 3123- 3129.

  • Lesperance f, Frasure- Smith N, Talajic M Major depression before and after myocardial infraction: its nature and consequences. Psychosom Med. 1996 (58), 99-110.

  • Lauzon C, Beck CA, Huynh T et al. Depression and prognosis following hospital admission because of acute myocardial infarction. CMAJ. 2003(108), 547-552.

  • Rumsfeld JS, Jones PG, Whooley M, et al. Depression predicts mortality and hospitalization in patients with myocardial infarction complicated by heart failure. Am Heart J. 2005 (150), 961-967.

  • Tridevi MH, Fava M, Wisniewski SR, et al. Evaluation of outcomes with citalopram for depression using measurementbased care in STAR*D: Implications for clinical practice. Am J Psychiatry. 2006 (163), 28-40.

  • Glassman AH, O’Connor CM, califf RM,et al. Sertraline treatment of major depression in patients with acute MI or unstable angina. JAMA. 2002 (288),701-709.

  • Swenson JR, O’Connor CM, Barton D, et al. Influence of depression and effect of treatment with sertraline on quality of life after hospitalization for acute coronary syndrome. Am J Cardiol. 2003 (92),1271-1276.

  • Whang W. Kubzansky LD, Kawachi I, Rexrode KM. Kroenke CH, Glynn RJ, Garan H, Albert CM. Depression and risk of sudden cardiac death and coronary heart disease in women: results from the Nurses' Health Study. J Am Coll Cardiol 2009 (53), 950-958.

  • Weeke P. Jensen A, Folke F, Gislason GH, Olesen JB, Andersson C, Fosbol EL, Larsen JK, Lippert FK, Nielsen SL, Gerds T, Andersen PK, Kanters JK, Poulsen HE, Pehrson S, Kober L, TorpPedersen C. Antidepressant use and risk of out-of-hospital cardiac arrest: a nationwide case-time-control study. Clin Pharmacol Ther 2012 (92), 72-79.

  • Patkar AA, Pae CU, Masand Ps. Transdermal selegiline: the new generation of monoamine oxidase inhibitors. CNS spectr: 2006 (11), 363-375.

  • Halper JP, Mann J. cardiovascular effect of antidepressants medication Br J Psych.1988; (Suppl):87-98.

  • Rutledge T, Redwine LS, Linke SE, Mills PJ. A meta-analysis of mental health treatments and cardiac rehabilitation for improving clinical outcomes and depression among patients with coronary heart disease Psychosom Med 2013 (75), 335-349.

  • Blumenthal JA, sherwood A, smith PJ, Watkins L, Mabe S, Kraus WE, Ingle K, Miller P, Hinderliter A. Enhancing cardiac rehabilitation with stress management training: a randomized, clinical efficacy. Circulation. 2016 (133), 1341-1350.


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  • Depression: As a Risk Factor for Coronary Heart Disease

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Authors

Marathe Varsha S.
Department of Pharmacology, P.S.G.V.P.M’s College of Pharmacy, Shahada. Department of Pharmacology, Ahinsa Institute of Pharmacy, Dondaicha, India
Azam Z. Shaikh
Department of Pharmacology, P.S.G.V.P.M’s College of Pharmacy, Shahada. Department of Pharmacology, Ahinsa Institute of Pharmacy, Dondaicha, India
S. P. Pawar
Department of Pharmacology, P.S.G.V.P.M’s College of Pharmacy, Shahada. Department of Pharmacology, Ahinsa Institute of Pharmacy, Dondaicha, India
Ritik. S. Jain
Department of Pharmacology, P.S.G.V.P.M’s College of Pharmacy, Shahada. Department of Pharmacology, Ahinsa Institute of Pharmacy, Dondaicha, India

Abstract


We conducted a review to resolve whether there is relationship between depression and coronary heart disease or not. Depression is a mental health problem which is spread widely and most of physicians are well acquainted with this concept of depression. Diagnosis of depression disorder based on continuity of illness, etiology of illness and number of symptoms - all these discriminations should be reported during inspecting the link between depression and coronary heart disease. We review the mechanism of linking depression and coronary heart disease i.e. relationship between depression and inflammation, depression and autonomic dysfunction, CHD and autonomic dysfunction, depression and Sleep architecture disruption, depression and circadian rhythm disruption, CHD and circadian rhythm disruption, and depression and behavioral mechanism. There is bidirectional association between depression and coronary artery disease i.e. coronary artery disease can cause major depressive disorder and depression is risk factor for CAD and its complications. Major depression is a devastating comorbid disease that can make recovery difficult and increase risk of cardiac mortality and morbidity. We also go over the therapy options like Psychotherapy, Electroconvulsive therapy, Exercise etc. But there are some antidepressant medications also available for treating depression in patients associated with CAD. The antidepressant medications like SSRIs e.g. Sertraline, fluoxetine, citalopram etc. appears to be safe in individual with depression and concomitant CAD or unstable angina. However, some evidence suggests that SSRIs like tricyclics, may increase risk cardiac events and death when taken for long time. New classes of antidepressants have dual reuptake inhibition for serotonin and nor-epinephrine e.g. venlafaxine. These medications are slightly more successful than SSRIs in treating depression, but they also have some adverse effects. Selegiline transdermal form was recently licensed for the treatment of MDD. Oral selegiline is not effective antidepressant. When compared to oral selegiline, STS results in stable plasma levels of drug and increased drug concentration in the brain.

Keywords


Coronary heart disease, Depression, CAD, Venlafaxine.

References