Sudden Cardiac Death Workup

Updated: Apr 28, 2014
  • Author: Ali A Sovari, MD, FACP, FACC; Chief Editor: Jeffrey N Rottman, MD  more...
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Workup

Laboratory Studies

Laboratory studies in the workup of sudden cardiac death include the following:

  • Cardiac enzymes (creatine kinase, myoglobin, troponin): Elevations in these enzyme levels may indicate ischemia and MI. The extent of myocardial damage usually can be correlated to the extent of elevation in the enzyme levels. Patients are at increased risk for arrhythmia in the peri-infarct period.
  • Electrolytes, calcium, and magnesium: Severe metabolic acidosis, hypokalemia, hyperkalemia, hypocalcemia, and hypomagnesemia are some of the conditions that can increase the risk for arrhythmia and sudden death.
  • Quantitative drug levels (quinidine, procainamide, tricyclic antidepressants, digoxin): Drug levels higher than the levels indicated in the therapeutic index may have a proarrhythmic effect. Subtherapeutic levels of these drugs in patients being treated for specific cardiac conditions also can lead to an increased risk for arrhythmia. Most of the antiarrhythmic medications also have a proarrhythmic effect.
  • Toxicology screen: Looking for drugs, such as cocaine, that can lead to vasospasm-induced ischemia is warranted if suspicion exists. Obtaining levels of drugs (antiarrhythmics) also may be warranted.
  • Thyroid-stimulating hormone: Hyperthyroidism can lead to tachycardia and tachyarrhythmias. Over a period of time, it also can lead to heart failure. Hypothyroidism can lead to QT prolongation.
  • Brain natriuretic peptide (BNP): BNP has predictive value especially in post MI patients and in patients with heart failure. Although preliminary and not conclusive, emerging data support the notion that an elevated BNP level may provide prognostic information on the risk of SCD, independent of clinical information and LVEF.
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Chest Rradiography

This may reveal whether someone is in congestive heart failure. It also can show signs suggesting LV enlargement or RV enlargement. Signs of pulmonary hypertension also may be evident on the chest radiograph.

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Echocardiography

Two-dimensional echocardiography with Doppler is essential in the evaluation of SCD. A number of studies have demonstrated that the use of 2-dimensional echocardiogram to evaluate left wall motion abnormalities after an acute MI (using the LV wall-motion score index) is useful in predicting the risk for major cardiac events, including sudden death. A decrease in the ejection fraction and worsening wall motion abnormalities upon exercise echocardiography in patients who have had an MI has been suggested to confer increased risk of cardiac death.

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Nuclear Imaging

Resting thallium or technetium-99m scintigraphy is helpful in assessing myocardial damage after MI. A larger defect has been associated with greater risk for future cardiac events. Exercise nuclear scintigraphy is very sensitive for detecting the presence, extent, and location of myocardial ischemia. Gibson et al found that pharmacologic-stress nuclear (dipyridamole or adenosine) scintigraphy was better than submaximal exercise ECG and coronary angiography in predicting cardiac death and other cardiac events. These tests can be very helpful in patients with low functional capacity such as chronic obstructive pulmonary disease, peripheral vascular disease, or orthopedic problems. The Multi-Center Post-Infarction Research Group provided evidence that resting ejection fraction was the most important noninvasive predictor of SCD and other cardiac events in patients with MI.

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Other Tests

Other diagnostic studies include the following:

  • Electrocardiogram: This study is indicated in all patients. Evidence of MI, prolonged QT interval, short QT interval, epsilon wave, Brugada sign, short PR, a WPW pattern, or other conditions should be sought.
  • Signal-averaged ECG (SAECG) has been variably reported to be useful in analysis of patients with SCD. What may be more useful is analysis of T-wave alternans in patients with VT, VF, and/or SCD. Small changes in T-amplitude are not detected in 12-lead ECG. Microvolt T wave alternans (MTWA) amplifies the alternans and may be used in the workup to predict the risk of SCD. MTWA appears to have high negative predictive value for the risk of SCD in patient with low LVEF (< 35%). [24] In addition, a pooled- analysis from 5 prospective studies showed that SCA happens in approximately 3% of patients with an abnormal MWTA test and LVEF >35%, suggesting that MTWA may be considered as a tool to identify patients at risk for SCA. [24] However, further studies are required to determine how MTWA alone or perhaps in combination with other electrophysiologic tools can be used to risk stratify the patients at risk for SCA.
  • Genetic testing: The value of genetic testing in conditions such as congenital long QT and HCM is still being evaluated. Some studies have recommended the testing of siblings and close relatives of people with SCD due to these conditions.
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Procedures

Coronary angiography

Perform cardiac catheterization in patients who survive SCD to assess the state of ventricular function and the severity and extent of CAD. The number of vessels with severe obstruction and the degree of LV dysfunction are important variables in predicting cardiac events. Ejection fraction is the best predictor of significant cardiac events and survival. Coronary angiography also can help identify coronary anomalies and other forms of congenital heart disease. Angiography is performed with the aim of identifying patients who may benefit from revascularization. Revascularization is indicated when ischemic myocardium is present as the underlying substrate of VT/VF.

Electrophysiology studies

In targeted patients, EPS play diagnostic, prognostic, and therapeutic roles. EPS usually are performed after ischemic and structural heart disease has been diagnosed and addressed. These studies have been used to identify patients who have inducible versus noninducible sustained monomorphic VT. The presence of inducible sustained VT, at baseline or when the patient is on antiarrhythmic medications, confers a higher risk for sudden death. Significantly lower ventricular function also has been observed in patients with inducible sustained VT. Inducible bundle-branch reentrant VT can be seen in patients with DCM and in the postoperative period after valvular replacement. As many as 20% of patients with HCM have inducible sustained monomorphic VT.

The identification of accessory pathways also is possible with these studies. EPS are performed with an eye toward the following:

  • Ablation of VT foci, eg, bundle branch VT, RVOT VT, and some cases of idiopathic LV tachycardia
  • ICD implantation, which is generally the case in survivors of SCD
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