We enjoyed reading the well-done and timely article by Espinoza et al . regarding the effect of therapeutic hypothermia on left ventricular function in an open-chest, anesthetized, and intubated porcine model. Using conventional two-dimensional echocardiography, hemodynamic monitoring, continuous epicardial ultrasonic measurement of the anterior cardiac wall thickness, and an electrocardiographic tracing, the authors compared the effect of baseline temperature (38°C) during spontaneous heart rate and during atrial pacing at 100 beats/min with that of a moderate degree of hypothermia (33°C) and the same heart rate parameters.

The authors found that conventional two-dimensional echocardiographic and hemodynamic parameters such as cardiac output, stroke volume, ejection fraction, longitudinal strain, end-diastolic pressure, wall dimensions, and midwall fractional shortening remained unchanged during hypothermia. However, the anterior wall thickening velocity in mid to late systole was reduced, systolic duration was prolonged, and the relative time spent in diastole was shortened during spontaneous heart rates and was absolutely shortened with atrial pacing during hypothermia. They also found that left ventricular filling shifted from early to late diastole, and because the pressure–wall thickness loop area (an indirect measure of wall stress) was reduced, they predicted a reduction in myocardial work. Corrected QT interval was not measured in the study.

The authors concluded that hypothermia caused reversible systolic and significant diastolic dysfunction at least in the porcine model during moderate hypothermia. They went on to provide a possible explanation for the left ventricular filling abnormality, namely, the direct effects of hypothermia on the myocytes and extracellular matrix, possibly causing an increase in wall stiffness.

QT-interval prolongation during therapeutic hypothermia is well described and is inversely related to the degree of hyperthermia. Myocardial function has been found to be abnormal in patients with congenital long-QT syndrome, and the echocardiographic findings resemble the authors’ findings in hypothermia. The majority of patients with long-QT syndrome have a delay in the mid to late systolic contraction velocity and a prolonged systolic duration. In high-risk symptomatic patients, postejection contraction, T-wave notching, and more severe prolongation of systole are found. Contraction duration in this cohort was significantly correlated to the corrected QT interval. In the authors’ study, it is interesting to see that T-wave notching and postejection contraction were seen in Figure 3B, and postejection contraction alone was seen in Figures 4 and 7 during hypothermia.

Myocardial dysfunction has also been shown to be echocardiographically evident in other conditions with prolonged QT intervals, such as drug-induced QT prolongation and that produced by right stellectomy in dogs. Cold saline blockade of the right stellate ganglion in dogs causes a reversible prolongation of the QT interval, prolonged systolic contraction, and delayed wall thickening velocity in mid to late systole.

We believe that a purely mechanical phenomenon may not be the only explanation for hypothermia’s effect on the myocardium but that an electric or sympathetic imbalance process could be a reasonable mechanism. QT-interval prolongation was evident in all of the figures in the article in which hypothermia was tested. The considerations of calcium channel aberrations causing action potential prolongation, QT-interval lengthening, prolonged systolic contraction with reduced wall thickening velocity, and truncation of diastolic duration with hypothermia are all quite reasonable. The reversal of this phenomenon in patients with long-QT syndrome using intravenous verapamil has been reported and may be worth studying in hypothermia.

We conclude that the finding of prolongation of systole with decreased mid to late systolic wall thickening and the truncation of diastole with therapeutic hypothermia may be related to the prolongation of the QT interval from electric alterations causing mechanical consequences.