Takotsubo cardiomyopathy
| Takotsubo cardiomyopathy | |
|---|---|
| Other names | Transient apical ballooning syndrome,[1] apical ballooning cardiomyopathy,[2] stress-induced cardiomyopathy, broken-heart syndrome, Gebrochenes-Herz syndrome[3] |
| Schematic representation of cardiomyopathy (A) compared to a normal heart (B) | |
| Specialty | Cardiology |
| Duration | Typically a few days, up to a few months |
| Risk factors | Physical stress (e.g., sepsis, chemotherapy), psychological stress (e.g., loss of employment, sudden loss of relationship, grief, anxiety), genetic predisposition |
| Prognosis | Good |
Takotsubo cardiomyopathy or takotsubo syndrome (TTS), also known as stress cardiomyopathy, is a type of non-ischemic cardiomyopathy in which there is a sudden temporary weakening of the muscular portion of the heart.[4] It usually appears after a significant stressor, either physical or emotional; when caused by the latter, the condition is sometimes called broken heart syndrome.[5]
Examples of physical stressors that can cause TTS are sepsis, shock, subarachnoid hemorrhage, and pheochromocytoma. Emotional stressors include bereavement, divorce, or the loss of a job.[6] Reviews suggest that of patients diagnosed with the condition, about 70–80% recently experienced a major stressor, including 41–50% with a physical stressor and 26–30% with an emotional stressor.[7][8] TTS can also appear in patients who have not experienced major stressors.[8][9]
The pathophysiology is not well understood, but a sudden massive surge of catecholamines such as adrenaline and noradrenaline from extreme stress or a tumor secreting these chemicals is thought to play a central role.[10] Excess catecholamines, when released directly by nerves that stimulate cardiac muscle cells, have a toxic effect and can lead to decreased cardiac muscular function or "stunning".[11][12] Further, this adrenaline surge triggers the arteries to tighten, thereby raising blood pressure and placing more stress on the heart, and may lead to spasm of the coronary arteries that supply blood to the heart muscle.[10] This impairs the arteries from delivering adequate blood flow and oxygen to the heart muscle.[10] Together, these events can lead to congestive heart failure and decrease the heart's output of blood with each squeeze.[10]
Takotsubo cardiomyopathy occurs worldwide.[11] The condition is thought to be responsible for 2% of all acute coronary syndrome cases presenting to hospitals.[11] Although TTS has generally been considered a self-limiting disease, spontaneously resolving over the course of days to weeks, contemporary observations show that "a subset of TTS patients may present with symptoms arising from its complications, e.g. heart failure, pulmonary edema, stroke, cardiogenic shock, or cardiac arrest". This does not imply that rates of shock/death of TTS are comparable to those of acute coronary syndrome, but that patients with acute complications may co-occur with TTS.[6] These cases of shock and death have been associated with the occurrence of TTS secondary to an inciting physical stressor such as hemorrhage, brain injury sepsis, pulmonary embolism or severe chronic obstructive pulmonary disease (COPD).[11]
It occurs more commonly in postmenopausal women.[11]
- ^ Eshtehardi P, Koestner SC, Adorjan P, Windecker S, Meier B, Hess OM, et al. (July 2009). "Transient apical ballooning syndrome--clinical characteristics, ballooning pattern, and long-term follow-up in a Swiss population". International Journal of Cardiology. 135 (3): 370–375. doi:10.1016/j.ijcard.2008.03.088. PMID 18599137.
- ^ Bergman BR, Reynolds HR, Skolnick AH, Castillo D (August 2008). "A case of apical ballooning cardiomyopathy associated with duloxetine". Annals of Internal Medicine. 149 (3): 218–219. doi:10.7326/0003-4819-149-3-200808050-00021. PMID 18678857.
- ^ Betts JG, Desaix P, Johnson E, Johnson JE, Korol O, Kruse D, et al. (29 July 2023). Anatomy & Physiology. Houston: OpenStax CNX. 19.4 Cardiac Physiology. ISBN 978-1-947172-04-3.
- ^ Zamir M (2005). The Physics of Coronary Blood Flow. Springer Science and Business Media. p. 387. ISBN 978-0387-25297-1.
- ^ "Mayo Clinic Research Reveals 'Broken Heart Syndrome' Recurs in 1 of 10 Patients". Medical News Today. MediLexicon International Ltd.
- ^ a b Ghadri JR, Wittstein IS, Prasad A, Sharkey S, Dote K, Akashi YJ, et al. (June 2018). "International Expert Consensus Document on Takotsubo Syndrome (Part I): Clinical Characteristics, Diagnostic Criteria, and Pathophysiology". European Heart Journal. 39 (22): 2032–2046. doi:10.1093/eurheartj/ehy076. PMC 5991216. PMID 29850871.
- ^ Sanchez-Jimenez EF (July 2013). "Initial clinical presentation of Takotsubo cardiomyopathy with-a focus on electrocardiographic changes: A literature review of cases". World Journal of Cardiology. 5 (7): 228–241. doi:10.4330/wjc.v5.i7.228. PMC 3722420. PMID 23888192.
- ^ a b Eitel I, von Knobelsdorff-Brenkenhoff F, Bernhardt P, Carbone I, Muellerleile K, Aldrovandi A, et al. (July 2011). "Clinical characteristics and cardiovascular magnetic resonance findings in stress (takotsubo) cardiomyopathy". JAMA. 306 (3): 277–286. doi:10.1001/jama.2011.992. PMID 21771988.
- ^ Templin C, Ghadri JR, Diekmann J, Napp LC, Bataiosu DR, Jaguszewski M, et al. (September 2015). "Clinical Features and Outcomes of Takotsubo (Stress) Cardiomyopathy". The New England Journal of Medicine. 373 (10): 929–938. doi:10.1056/NEJMoa1406761. PMID 26332547.
- ^ a b c d Tavazzi G, Zanierato M, Via G, Iotti GA, Procaccio F (December 2017). "Are Neurogenic Stress Cardiomyopathy and Takotsubo Different Syndromes With Common Pathways?: Etiopathological Insights on Dysfunctional Hearts". JACC. Heart Failure. 5 (12): 940–942. doi:10.1016/j.jchf.2017.09.006. PMID 29191302.
- ^ a b c d e Akashi YJ, Nef HM, Lyon AR (July 2015). "Epidemiology and pathophysiology of Takotsubo syndrome". Nature Reviews. Cardiology. 12 (7): 387–397. doi:10.1038/nrcardio.2015.39. hdl:10044/1/25730. PMID 25855605. S2CID 24742760.
- ^ Pelliccia F, Kaski JC, Crea F, Camici PG (June 2017). "Pathophysiology of Takotsubo Syndrome". Circulation. 135 (24): 2426–2441. doi:10.1161/CIRCULATIONAHA.116.027121. PMID 28606950. S2CID 207581288.