Review article: Utility of troponin after syncope: A systematic review and meta‐analysis

Stark, Claire Brigid; Smit, De Villiers; Mitra, Biswadev

doi:10.1111/1742-6723.12937

Cited by 4 publications

(2 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, such determinations are highly non-specific and rarely contribute to a certain diagnosis, and they may indicate serious illness rather than myocardial ischemia or heart failure. Therefore, it remains unclear whether they should be determined on a routine basis[ 88 ].…”

Section: Diagnostic Approach and Testmentioning

confidence: 99%

Arrhythmic syncope: From diagnosis to management

Pascual¹,

Marchite²,

Silva³

et al. 2023

World J Cardiol

View full text Add to dashboard Cite

Syncope is a concerning symptom that affects a large proportion of patients. It can be related to a heterogeneous group of pathologies ranging from trivial causes to diseases with a high risk of sudden death. However, benign causes are the most frequent, and identifying high-risk patients with potentially severe etiologies is crucial to establish an accurate diagnosis, initiate effective therapy, and alter the prognosis. The term cardiac syncope refers to those episodes where the cause of the cerebral hypoperfusion is directly related to a cardiac disorder, while arrhythmic syncope is cardiac syncope specifically due to rhythm disorders. Indeed, arrhythmias are the most common cause of cardiac syncope. Both bradyarrhythmia and tachyarrhythmia can cause a sudden decrease in cardiac output and produce syncope. In this review, we summarized the main guidelines in the management of patients with syncope of presumed arrhythmic origin. Therefore, we presented a thorough approach to syncope work-up through different tests depending on the clinical characteristics of the patients, risk stratification, and the management of syncope in different scenarios such as structural heart disease and channelopathies.

show abstract

Section: Diagnostic Approach and Testmentioning

confidence: 99%

Arrhythmic syncope: From diagnosis to management

Pascual¹,

Marchite²,

Silva³

et al. 2023

World J Cardiol

View full text Add to dashboard Cite

show abstract

“…Troponin levels may also be raised in conditions other than MI, and raised levels associated with these etiologies have also been associated with increased mortality [76]. It has been postulated that elevated troponin may indicate serious illness rather than MI alone [77]. Renal failure, sepsis, pulmonary embolism, burns and amyloidosis, for example, are also associated with elevated troponin [78].…”

Section: Atherosclerotic Plaque Stabilizationmentioning

confidence: 99%

Current Concepts in the Prevention of Perioperative Myocardial Injury

Bohringer¹,

Liu²

2020

Transl Perioper & Pain Med

View full text Add to dashboard Cite

Perioperative myocardial injury is frequently caused by tachycardia from excessive sympathetic nervous system activity resulting from the surgical stimulation (type 2) rather than by rupture of atherosclerotic plaques with superimposed thrombosis (type 1). The elevated sympathetic nervous system activity results in tachycardia that induces demand ischemia within the myocardium and damages the heart muscle. A rise in troponin has been shown to be a reliable predictor of adverse cardiovascular events when measured in a population at risk. This holds true even when the troponin rise is isolated and other markers for myocardial damage like prolonged ischemic type chest pain, new electrocardiogram changes or evidence of new myocardial damage on echocardiography and other cardiac imaging studies are absent. Treatments that prevent tachycardia by successfully controlling elevated sympathetic tone, like dexmedetomidine and thoracic epidural blockade with local anesthetic reduce troponin release and have been shown to prevent myocardial damage. Intravenous lidocaine and magnesium can also prevent tachycardia. Beta blockers reduce myocardial injury, but are associated with an increase in hypotension and ischemic stroke. Any method of attenuating sympathetic nervous system activity, may however, require treatment with intravenous fluids and vasopressors to prevent hypotension. Rupture of atherosclerotic plaques with superimposed coronary thrombosis is a far less common cause of myocardial infarction in the perioperative period than elevated sympathetic tone. This explains why prophylactic statins in previously statin-naïve patients do not reduce major adverse cardiovascular event rates. Antiplatelet agents are also ineffective in reducing adverse cardiovascular events in the perioperative period. Clinicians, therefore, need to focus their attention on heart rate control and the attenuation of the stress response to surgery, rather than on atherosclerotic plaque stability and antiplatelet drugs in order to successfully prevent perioperative myocardial injury.

show abstract