Dyspnea in a 63-Year-Old Who Had Heart Surgery as a Child

Sarah Blissett, MD, MHPE; Punag Divanji, MD; Harsh Agrawal, MD; Vaikom S. Mahadevan, MD; Elyse Foster, MD


December 09, 2019

Clinicians should seek to identify the cause of LV dysfunction, considering acquired or congenital etiologies. Acquired causes of LV dysfunction should be evaluated, including coronary artery disease, diabetes, alcohol, thyroid abnormalities, iron overload states, and tachycardia-mediated cardiomyopathy.

Coronary artery disease should not be overlooked in patients with congenital heart disease. In a Dutch cohort study, 80% of adults with congenital heart disease also had at least one cardiovascular risk factor.[7] Compared with women, men were more likely to smoke, with 24% using tobacco, and were more likely to have hypertension.[7] Data from Europe and the United Kingdom suggest the prevalence of diabetes is at least similar to the prevalence seen in the general population, with one study demonstrating a higher prevalence of diabetes in patients with congenital heart disease.[8] The rate of myocardial infarction in patients with repaired tetralogy of Fallot is similar to that in the general population.[9]

Once acquired causes are excluded, consideration can be given to LV dysfunction as it relates to sequelae of repaired tetralogy of Fallot. Several clinical variables have been associated with LV dysfunction as it relates to repaired tetralogy of Fallot. These include the following[4,5,6]:

The association with decreased RV function, RV dilation, and significant pulmonary regurgitation highlights the ventriculo-ventricular interactions between the RV and LV as a contributor in the pathophysiology of LV dysfunction in repaired tetralogy of Fallot. The QRS duration highlights the contribution of electromechanical dyssynchrony. Longer durations of palliative shunts, particularly Waterston (ascending aorta to pulmonary artery) and Potts (descending aorta to pulmonary artery) shunts, impose a volume load on the LV that could contribute to dysfunction. A greater number of surgical procedures, particularly in older patients who underwent surgeries with older bypass techniques, may contribute to LV owing to inadequate coronary protection during the surgical procedures.

Coronary artery disease was considered first in determining the etiology of heart failure for this patient in this case. Invasive coronary angiography was selected to evaluate for ischemia, given the multiple cardiovascular risk factors. Coronary angiography demonstrated a 95% obstructive lesion in the ostium of the left anterior descending artery. The LV dysfunction was felt to be out of proportion to the degree of coronary disease, particularly given the global hypokinesis identified, raising the possibly of a concomitant nonischemic contributor. Contributions from factors associated with repaired tetralogy of Fallot were suspected, given the presence of clinical features described to be involved in the pathophysiology of LV dysfunction in these patients, including male gender, longer QRS duration, and history of arrhythmia. Thus, the patient's LV dysfunction was thought to be due to coronary disease and sequelae of repaired tetralogy of Fallot.


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