troponin elevation in normal coronaries

8/7/2019 Troponin elevation in Normal Coronaries

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Troponin elevation in Coronary Vs.Non-Coronary Disease

Dr Haroon Rashid- ResidentDr Kakhaber Etsadashvili

Department of CardiologyCardiology Clinic Guli


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Q uestion

How good is Troponin T or I to rule out acute coronary syndrome in theemergency room when a patient

presents within two to three hours after the onset of symptoms ? 1. Very useful2. Useful

3. Rarely useful4. Not useful5. Not at all useful


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Introduction

Cardiac troponins (cTn) are the mostsensitive and specific biochemical markersof myocardial injury and with the new high-

sensitivity troponin methods very minor damages on the heart muscle can bedetected.

However, elevated cTn levels indicatecardiac injury, but do not define the causeof the injury.

Thus, cTn elevations are common in manydisease states and do not necessarilyindicate the presence of a thrombotic

acute coronary syndrome (ACS).


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Introduction

The aim of this presentation is to reviewdata from studies of non-ACS patients withacutely elevated troponin who in clinical

practice may be difficult to discriminatefrom ACS patients. There are no guidelines to treat patients

with elevated cTn levels and no coronarydisease.


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Introduction The ESC/ACCF/AHA/WHF task force for the

redenition of M I agreed on the followingdenition of M I;

Detection of rise and/or fall of cardiac

biomarkers (preferably troponin) above the 99thpercentile of the upper reference limit together with evidence of ischaemia with at least one of the following: Ischaemic symptoms, Electrocardiography (ECG) changes of new

ischaemia, development of pathologic Q -waves in theECG or

Imaging evidence of new loss of viable myocardiumor new regional wall motion abnormality.


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Causes for TroponinElevations

R easons for Acute Troponin elevation

Acute coronary syndrome

Acute heart failure

Pulmonary embolismStroke

Acute aortic dissection

Tachyarrhythmias

Hypotension/shock

Sepsis

ARDS

Perimyocarditis

Endocarditis

Taka-tsubo cardiomyopathyRadiofrequency catheter ablation

Cardiac contusion

Strenuous exercise

Sympathomimetic drugs

Chemotherapy


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Troponin Assays

ESC/ACCF/AHA/WHF infarct denitiongives no recommendations for use of the99th percentile value for risk assessment.

However, measurements were made withcTn assays with an imprecision 20%. Only for the subset of patients with end-

stage renal disease (ESRD), the NACBguidelines have recommended a changein the cTn concentration of 20% for thediagnosis of M I in those who present withelevated cTn, 69 h after presentation.


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TachycardiasIn clinical practice, elevated troponinconcentrations are some-times observedafter prolonged episodes of supraventricular tacharrhythmias (SVT),even in presumably healthy individuals.

The most likely mechanism for troponinelevation following tachycardia may beshortening of diastole with subsequentsubendocardial ischaemia.


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Acute Heart Failure

Reasons for higher prevalence of cTnT inacute HF are still unsettled.It has been speculated that increased

ventricular preload causing myocardialstrain may cause troponin release.


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Pericarditis and Myocarditis

Despite the fact that troponins are notpresent in the pericardium, cTn has beenreported to be elevated in 3249% of cases of acute pericarditis, as aconsequence of the involvement of theepicardium in the inammatory processs.

Troponin elevations reect myocardiallesion, thus an acute pericarditis withsigns of myocarditis (evidenced by globalor regional myocardial dysfunction or elevated cTn) is called myopericarditis.


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Acute Pulmonary Embolism

The reason for cTn release in PE is still unclear. The acute right ventricular strains secondary

to increase in pulmonary artery resistancemay cause a troponin elevation in PE. However, another explanation to an

elevated troponin in PE patients might behypoxaemia due to perfusionventilationmismatch, hypoperfusion as a consequenceof low output and reduced coronary bloodow, as well as paradoxical embolism fromsystemic veins to the coronary arteries,usually via a patent foramen ovale.


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Tako-tsubo

Tako-tsubo cardiomyopathy has beencalled stress-induced cardiomyopathy,broken heart syndrome or transient leftventricular apical ballooning syndrome.

Tako-tsubo cardiomyopathy have beenproposed, including catecholamineinduced myocardial stunning, ischaemia-mediated stunning due to multivesselepicardial or microvascular spasm,aborted acute myocardial infarction (AM I),and focal myocarditis.


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Sepsis

Approximately 50% of patients with severesepsis and septic shock may developimpairment of ventricular performance.

Elevations in cTn correlate with thepresence of left ventricular systolicdysfunction.


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StrokeIncreases in cTn have been reported in alltypes of stroke [ischaemic, intracerebralhaemorrhage, and subarachnoidhaemorrhage (SAH)].

Also contractile dysfunction and ECGchanges such as ST-segment depressionand T-wave inversion (STT changes) arecommon in stroke patients.

Left-ventricular systolic dysfunction hasbeen observed in all three kinds of strokes.


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StrokeIt has also been proposed that theobserved cardiac abnormalities are

secondary to increased/disturbedsympathetic activity prooked by acutestroke.

An exaggerated catecholamine releasemay lead to excessive release of intracellular calcium ions and subsequentreversible myocyte dysfunction.

Alternate explanation is that thecatecholamine surge acts as anuncontrolled severe myocardial stresstest, which essentially reveals stablecoronary plaques.


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Strenuous exerciseIn untrained indiviuals, prolonged exerciseinduces a state of muscular fatigue.Involvement of cardiac muscle in thisprocess is manifested as transientlydecreased systolic and diastolic function,so-called cardiac fatigue.

Therefore, it has been hypothesized thattroponin is released due to degradation of cytosolic troponin or increasedpermeability of the cell membranes of myocytes under stress.


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Cardiac Contusion

Troponins may be elevated after thoracictrauma.

CPR

Cardioversion


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Summary


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Take home message

Acute coronary syndrome is a syndrome,defined as myocardial cell death due toprolonged myocardial ischemia.

Cardiac troponins (cTn) are the mostsensitive and specic biochemical markersof myocardial injury and with the new high-sensitivity troponin methods very minor damages on the heart muscle can bedetected.

However, elevated cTn levels indicatecardiac injury, but do not dene the causeof the injury.


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Take home messageIn the clinical work it may be difcult tointerpret dynamic changes of troponin inconditions such as stroke, pulmonaryembolism, sepsis, acute perimyocarditis,Tako-tsubo, acute heart failure, andtachycardia.

There are no guidelines to treat patientswith elevated cTn levels and no coronarydisease.

The current strategy of treatment of patients with elevated troponin and non-acute coronary syndrome involves treating

the underlying causes.


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Can we afford to miss a diagnosis of acutecoronary syndrome in the emergency room ?

We know 20% of ACS can be totally silent. Some produce very vague symptoms

especially in elderly and diabetics.

In spite of the highest awareness andavailability of scientific expertise,knowledge base the error rate of diagnosing ACS stands at an astonishing58%.

Out of 10500 patients with suspectedACS. Only 17 % had real ACS. 55% wereadmitted initially as ACS later turned outto be non cardiac


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Can we afford to miss a diagnosis of acute coronarysyndrome in the emergency room ?

Definitely not . . .but do we succeed inthat ? The answer is same definitely not

We need to realise with even with a 55%

of false positive initial diagnosis 2% realACS escape net !The only fool proof method for not missing, even a singlecase of ACS is to label every patient withchest pain as ACS .


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Conclude

In this vexing issue, we should realize, infield of medical decision making errors due to acts of commission ( Making an inappropriate drug/procedure/surgery is easily accepted by medical professionals as well as the court of law!).But acts of omission, like missing adiagnosis or failure to prescribe a drug or

perform a procedure is rarely accepted and is considered a great negligenceand bring intense guilty feeling among thephysicians .


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Hippocrates got it right over 2000 years ago .

Primum non nocere-

(First let us do no harm)

troponin elevation in normal coronaries

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