Int J Angiol
DOI: 10.1055/s-0044-1782602
Review Article

Menstruation-Related Angina—The Wee Hours

Sandy Goyette
1   American University School of Medicine Aruba, Oranjestad, Aruba
,
Tulika Mishra
2   Department of Microbiology and Immunology, American University School of Medicine Aruba, Oranjestad, Aruba
,
Farah Raza
1   American University School of Medicine Aruba, Oranjestad, Aruba
,
Zahra Naqvi
1   American University School of Medicine Aruba, Oranjestad, Aruba
,
Sarah Khan
1   American University School of Medicine Aruba, Oranjestad, Aruba
,
Abrar Khan
3   Department of Anatomy and Dean of Basic Sciences, American University School of Medicine Aruba, Oranjestad, Aruba
,
Pamphil Igman
4   Department of Preventive Medicine and Biostatistics, American University School of Medicine Aruba, Oranjestad, Aruba
,
Malpe Surekha Bhat
5   Department of Biochemistry and Molecular Biology and Basic Medical Research, American University School of Medicine Aruba, Oranjestad, Aruba
› Author Affiliations

Abstract

Literature reveals two kinds of menstruation-related anginas—cardiac syndrome X (CSX) and catamenial angina. CSX generally occurs in perimenopausal or postmenopausal women; catamenial angina affects females from puberty to menopause with existing/preexisting or predisposed to coronary artery disease. CSX involves recurring anginal-type retrosternal chest pains during exercise or rest with no significant findings on angiogram. Catamenial angina is menstruation-associated recurrent nonexertional left-sided chest pain alongside diaphoresis, hot flushes, and persistent lethargy. Pathophysiology of both anginas revolve around decreased levels of estrogen. Estrogen is known to act via genomic and nongenomic pathways on cardiomyocytes, endothelial cells, and smooth muscle cells to exert its cardioprotective effect. These cardioprotective effects could be lost during the postovulation phase and at the end of menstruation as well as during perimenopause or menopause owing to the decreased levels of estrogen. Evaluation should begin with a history and physical examination and focus on noninvasive tests such as exercise tolerance test, electrocardiogram, and echocardiogram. Reducing symptoms that cause discomfort and improving quality of life should be the main goal in management. Nitrates along with β blockers and analgesics for pain are the main pharmacologic modalities. Exercise training, smoking cessation, weight loss, and dietary changes are nonpharmacological modalities. Proper awareness and effective communication with patients or caregivers can lead to early diagnosis and treatment initiation.



Publication History

Article published online:
15 March 2024

© 2024. International College of Angiology. This article is published by Thieme.

Thieme Medical Publishers, Inc.
333 Seventh Avenue, 18th Floor, New York, NY 10001, USA

 
  • References

  • 1 Mahtani AU, Padda IS, Johal GS. Cardiac syndrome X. [Updated December 12, 2022]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023
  • 2 Piegza M, Wierzba D, Piegza J. Cardiac syndrome X - the present knowledge. Psychiatr Pol 2021; 55 (02) 363-375
  • 3 Qi Y, Li L, Feng G, Shao C, Cai Y, Wang Z. Research progress of imaging methods for detection of microvascular angina pectoris in diabetic patients. Front Cardiovasc Med 2021; 8: 713971
  • 4 Huang C, Lin B, Yuan Y. et al. Associations of menstrual cycle regularity and length with cardiovascular diseases: a prospective study from UK Biobank. J Am Heart Assoc 2023; 12 (11) e029020
  • 5 Case AM, Reid RL. Effects of the menstrual cycle on medical disorders. Arch Intern Med 1998; 158 (13) 1405-1412
  • 6 Ueno A, Yoshida T, Yamamoto Y, Hayashi K. Successful control of menstrual cycle-related exacerbation of inflammatory arthritis with GnRH agonist with add-back therapy in a patient with rheumatoid arthritis. J Obstet Gynaecol Res 2022; 48 (07) 2005-2009
  • 7 Pati GK, Kar C, Narayan J. et al. Irritable bowel syndrome and the menstrual cycle. Cureus 2021; 13 (01) e12692
  • 8 Choo WK. Menstruation angina: a case report. J Med Case Rep 2009; 3: 6618-6621
  • 9 Jones E, Eteiba W, Merz NB. Cardiac syndrome X and microvascular coronary dysfunction. Trends Cardiovasc Med 2012; 22 (06) 161-168
  • 10 Agrawal S, Mehta PK, Bairey Merz CN. Cardiac syndrome X: update 2014. Cardiol Clin 2014; 32 (03) 463-478
  • 11 Tweet MS, Codsi E, Best PJM, Gulati R, Rose CH, Hayes SN. Menstrual chest pain in women with history of spontaneous coronary artery dissection. J Am Coll Cardiol 2017; 70 (18) 2308-2309
  • 12 Lloyd GW, Patel NR, McGing E, Cooper AF, Brennand-Roper D, Jackson G. Does angina vary with the menstrual cycle in women with premenopausal coronary artery disease?. Heart 2000; 84 (02) 189-192
  • 13 dos Santos RL, da Silva FB, Ribeiro Jr RF, Stefanon I. Sex hormones in the cardiovascular system. Horm Mol Biol Clin Investig 2014; 18 (02) 89-103
  • 14 Al Fatly Z, Beckers FLM, Sjauw KD, Roeters van Lennep JE, Schreuder MM. Catamenial chest pain and spontaneous coronary artery dissection: a case report. Case Rep Womens Health 2020; 28: e00256
  • 15 Gilhofer TS, Saw J. Spontaneous coronary artery dissection: a review of complications and management strategies. Expert Rev Cardiovasc Ther 2019; 17 (04) 275-291
  • 16 Singh M, Singh S, Arora R, Khosla S. Cardiac syndrome X: current concepts. Int J Cardiol 2010; 142 (02) 113-119
  • 17 Fladseth K, Lindekleiv H, Nielsen C. et al. Low pain tolerance is associated with coronary angiography, coronary artery disease, and mortality: the Tromsø study. J Am Heart Assoc 2021; 10 (22) e021291
  • 18 Yildirim M, Oztekin O, Oztekin D. et al. Recurrent chest pain, as a presenting sign of ovarian endometrioma. ISRN Surg 2011; 2011: 837501
  • 19 Narula N, Ngu S, Avula A, Mansour W, Chalhoub M. Left-sided catamenial pneumothorax: a rare clinical entity. Cureus 2018; 10 (05) e2567
  • 20 Kawano H, Motoyama T, Ohgushi M, Kugiyama K, Ogawa H, Yasue H. Menstrual cyclic variation of myocardial ischemia in premenopausal women with variant angina. Ann Intern Med 2001; 135 (11) 977-981
  • 21 Shimokawa H, Morishige K, Miyata K. et al. Long-term inhibition of Rho-kinase induces a regression of arteriosclerotic coronary lesions in a porcine model in vivo. Cardiovasc Res 2001; 51 (01) 169-177
  • 22 Loba RA, Gershenson DM, Lentz GM. et al. The menstrual cycle. Comprehensive Gynecology. 7th ed. Philadelphia: Elsevier Health Sciences; 2017: 93-104
  • 23 Mosca L, Banka CL, Benjamin EJ. et al; Expert Panel/Writing Group, American Academy of Physician Assistants, American Association for Clinical Chemistry, American Association of Cardiovascular and Pulmonary Rehabilitation, American College of Chest Physicians, American College of Emergency Physicians, American Diabetes Association, American Geriatrics Society, American Society for Preventive Cardiology, American Society of Echocardiography, American Society of Nuclear Cardiology, Association of Women's Health, Obstetric and Neonatal Nurses, Global Alliance for Women's Health, Mended Hearts, Inc, National Black Nurses Association, National Black Women's Health Imperative, National Women's Health Resource Center, North American Menopause Society, Partnership for Gender-Specific Medicine at Columbia University, Preventive Cardiovascular Nurses Association, Society for Vascular Medicine and Biology, Society for Women's Health Research, Society of Geriatric Cardiology, Women in Thoracic Surgery, WomenHeart: the National Coalition for Women with Heart Disease. Evidence-based guidelines for cardiovascular disease prevention in women: 2007 update. J Am Coll Cardiol 2007; 49 (11) 1230-1250
  • 24 Gerber Y, Weston SA, Redfield MM. et al. A contemporary appraisal of the heart failure epidemic in Olmsted County, Minnesota, 2000 to 2010. JAMA Intern Med 2015; 175 (06) 996-1004
  • 25 Dewan P, Rørth R, Jhund PS. et al. Differential impact of heart failure with reduced ejection fraction on men and women. J Am Coll Cardiol 2019; 73 (01) 29-40
  • 26 Brouwers FP, Hillege HL, van Gilst WH, van Veldhuisen DJ. Comparing new onset heart failure with reduced ejection fraction and new onset heart failure with preserved ejection fraction: an epidemiologic perspective. Curr Heart Fail Rep 2012; 9 (04) 363-368
  • 27 Han SH, Bae JH, Holmes Jr DR. et al. Sex differences in atheroma burden and endothelial function in patients with early coronary atherosclerosis. Eur Heart J 2008; 29 (11) 1359-1369
  • 28 Rattanasopa C, Phungphong S, Wattanapermpool J, Bupha-Intr T. Significant role of estrogen in maintaining cardiac mitochondrial functions. J Steroid Biochem Mol Biol 2015; 147: 1-9
  • 29 Sbert-Roig M, Bauzá-Thorbrügge M, Galmés-Pascual BM. et al. GPER mediates the effects of 17β-estradiol in cardiac mitochondrial biogenesis and function. Mol Cell Endocrinol 2016; 420: 116-124
  • 30 El Khoudary SR, Aggarwal B, Beckie TM. et al; American Heart Association Prevention Science Committee of the Council on Epidemiology and Prevention; and Council on Cardiovascular and Stroke Nursing. Menopause transition and cardiovascular disease risk: implications for the timing of early prevention: a scientific statement from the American Heart Association. Circulation 2020; 142 (25) e506-e532
  • 31 Furukawa T, Kurokawa J. Non-genomic regulation of cardiac ion channels by sex hormones. Cardiovasc Hematol Disord Drug Targets 2008; 8 (04) 245-251
  • 32 Patten RD, Pourati I, Aronovitz MJ. et al. 17β-estradiol reduces cardiomyocyte apoptosis in vivo and in vitro via activation of phospho-inositide-3 kinase/Akt signaling. Circ Res 2004; 95 (07) 692-699
  • 33 Shen T, Ding L, Ruan Y. et al. SIRT1 functions as an important regulator of estrogen-mediated cardiomyocyte protection in angiotensin II-induced heart hypertrophy. Oxid Med Cell Longev 2014; 2014: 713894
  • 34 Wang L, Tang ZP, Zhao W. et al. MiR-22/Sp-1 links estrogens with the up-regulation of cystathionine gamma-lyase in myocardium, which contributes to estrogenic cardioprotection against oxidative stress. Endocrinology 2015; 156 (06) 2124-2137
  • 35 dos Santos RL, da Silva FB, Ribeiro Jr RF, Stefanon I. Sex hormones in the cardiovascular system. Horm Mol Biol Clin Investig 2014; 18 (02) 89-103
  • 36 Dubey RK, Jackson EK. Estrogen-induced cardiorenal protection: potential cellular, biochemical, and molecular mechanisms. Am J Physiol Renal Physiol 2001; 280 (03) F365-F388
  • 37 Haynes MP, Li L, Sinha D. et al. Src kinase mediates phosphatidylinositol 3-kinase/Akt-dependent rapid endothelial nitric-oxide synthase activation by estrogen. J Biol Chem 2003; 278 (04) 2118-2123
  • 38 Scotland RS, Madhani M, Chauhan S. et al. Investigation of vascular responses in endothelial nitric oxide synthase/cyclooxygenase-1 double-knockout mice: key role for endothelium-derived hyperpolarizing factor in the regulation of blood pressure in vivo. Circulation 2005; 111 (06) 796-803
  • 39 Brosnihan KB, Li P, Figueroa JP, Ganten D, Ferrario CM. Estrogen, nitric oxide, and hypertension differentially modulate agonist-induced contractile responses in female transgenic (mRen2)27 hypertensive rats. Am J Physiol Heart Circ Physiol 2008; 294 (05) H1995-H2001
  • 40 Santos RL, Marin EB, Gonçalves WL, Bissoli NS, Abreu GR, Moysés MR. Sex differences in the coronary vasodilation induced by 17 β-oestradiol in the isolated perfused heart from spontaneously hypertensive rats. Acta Physiol (Oxf) 2010; 200 (03) 203-210
  • 41 Sobrino A, Oviedo PJ, Novella S. et al. Estradiol selectively stimulates endothelial prostacyclin production through estrogen receptor-alpha. J Mol Endocrinol 2010; 44 (04) 237-246
  • 42 Sickinghe AA, Korporaal SJA, den Ruijter HM, Kessler EL. Estrogen contributions to microvascular dysfunction evolving to heart failure with preserved ejection fraction. Front Endocrinol (Lausanne) 2019; 10: 442
  • 43 Orshal JM, Khalil RA. Gender, sex hormones, and vascular tone. Am J Physiol Regul Integr Comp Physiol 2004; 286 (02) R233-R249
  • 44 Ghisletti S, Meda C, Maggi A, Vegeto E. 17beta-estradiol inhibits inflammatory gene expression by controlling NF-kappaB intracellular localization. Mol Cell Biol 2005; 25 (08) 2957-2968
  • 45 Dai Q, Likes III CE, Luz AL. et al. A mitochondrial progesterone receptor increases cardiac beta-oxidation and remodeling. J Endocr Soc 2019; 3 (02) 446-467
  • 46 Lan C, Cao N, Chen C. et al. Progesterone, via yes-associated protein, promotes cardiomyocyte proliferation and cardiac repair. Cell Prolif 2020; 53 (11) e12910
  • 47 Simoncini T, Mannella P, Fornari L. et al. Differential signal transduction of progesterone and medroxyprogesterone acetate in human endothelial cells. Endocrinology 2004; 145 (12) 5745-5756
  • 48 You Y, Tan W, Guo Y. et al. Progesterone promotes endothelial nitric oxide synthase expression through enhancing nuclear progesterone receptor-SP-1 formation. Am J Physiol Heart Circ Physiol 2020; 319 (02) H341-H348
  • 49 Smiley DA, Khalil RA. Estrogenic compounds, estrogen receptors and vascular cell signaling in the aging blood vessels. Curr Med Chem 2009; 16 (15) 1863-1887
  • 50 Wassmann K, Wassmann S, Nickenig G. Progesterone antagonizes the vasoprotective effect of estrogen on antioxidant enzyme expression and function. Circ Res 2005; 97 (10) 1046-1054
  • 51 Tezuka A, Shiina K, Fujita Y. et al. Efficacy of combined estrogen-progestin hormone contraception therapy for refractory coronary spastic angina in very young women. J Cardiol Cases 2020; 21 (05) 200-203
  • 52 Huang Q, Wang WT, Wang SS, Pei A, Sui XQ. Cardiovascular magnetic resonance image analysis and mechanism study for the changes after treatments for primary microvascular angina pectoris. Medicine (Baltimore) 2021; 100 (21) e26038
  • 53 Adachi Y, Ikeda N, Sakakura K. et al. Intractable coronary spastic angina improvement after continuous combined estrogen-progestin hormonal contraception use in a premenopausal woman. Intern Med 2016; 55 (18) 2639-2642
  • 54 Carvajal JA, Germain AM, Huidobro-Toro JP, Weiner CP. Molecular mechanism of cGMP-mediated smooth muscle relaxation. J Cell Physiol 2000; 184 (03) 409-420
  • 55 Zhao Y, Vanhoutte PM, Leung SW. Vascular nitric oxide: beyond eNOS. J Pharmacol Sci 2015; 129 (02) 83-94
  • 56 Webb RC. Smooth muscle contraction and relaxation. Adv Physiol Educ 2003; 27 (1-4): 201-206
  • 57 Kukovetz WR, Holzmann S, Pöch G. Molecular mechanism of action of nicorandil. J Cardiovasc Pharmacol 1992; 20 (Suppl. 03) S1-S7
  • 58 Barbato JC. Nicorandil: the drug that keeps on giving. Hypertension 2005; 46 (04) 647-648
  • 59 Gorre F, Vandekerckhove H. Beta-blockers: focus on mechanism of action. Which beta-blocker, when and why?. Acta Cardiol 2010; 65 (05) 565-570
  • 60 Rehsia NS, Dhalla NS. Mechanisms of the beneficial effects of beta-adrenoceptor antagonists in congestive heart failure. Exp Clin Cardiol 2010; 15 (04) e86-e95
  • 61 Elliott WJ, Ram CVS. Calcium channel blockers. J Clin Hypertens (Greenwich) 2011; 13 (09) 687-689
  • 62 Stewart LK, Kline JA. Fibrinolytics for the treatment of pulmonary embolism. Transl Res 2020; 225: 82-94
  • 63 Mangiacapra F, Viscusi MM, Verolino G. et al. Invasive assessment of coronary microvascular function. J Clin Med 2021; 11 (01) 228