Transient Local Changes in Right Ventricular Monophasic Action Potentials Due to Ajmaline in a Patient with Brugada Syndrome

A 48-year-old patient with recurrent episodes of palpitations and syncope presented with transient ST segment elevation in the right precordial ECG leads. Structural heart disease was excluded. No arrhythmias were inducible by programmed ventricular stimulation. Parallel to ST elevation after intravenous ajmaline, a gradual and reversible delay in the upstroke of right ventricular (RV) monophasic action potentials (MAPs) occurred that was most marked in the RV outflow tract and nearly absent at right free-wall recordings. Ajmaline led to a cycle length-dependent increase in RV dispersion of repolarization. Thus, right endocardial MAPs may demonstrate regionally different action potential changes that may contribute to the ECG changes in Brugada syndrome.     

Evaluation of nonischemic cardiomyopathies using cardiovascular magnetic resonance

Conclusion  A single CMR examination provides unparalleled information regarding various forms of cardiomyopathy and specifically allows for accurate assessment with regard to etiology and prognosis and helps guide decisions regarding therapy and risk stratification. Given its increasing availability, CMR is likely to play a bigger role in the investigation and risk stratification of patients in the future. Scan times are also shortening, and 3-T scanners now offer better spatial and temporal resolution than ever before.     

Angiotensin-Converting Enzyme Inhibitors Potentiate Preconditioning Through Bradykinin B2 Receptor Activation in Human Heart

Objectives. This study was designed to determine whether angiotensin-converting enzyme (ACE) inhibitors play a role in cardioprotection in a human model of preconditioning.

Background. Recent studies have suggested that bradykinin may contribute to the protective effects of preconditioning in animal models. ACE inhibitors are known to inhibit the degradation of bradykinin and hence may be able to potentiate the effect of preconditioning.

Methods. We examined the effects of the ACE inhibitors captopril and lisinopril in combination with a subthreshold preconditioning stimulus (i.e., insufficient to have any protective effects alone). Human atrial trabeculae were superfused with Krebs buffer and paced at 1 Hz. They were subjected to a full or subthreshold preconditioning stimulus consisting of either 3 or 1.5 min of simulated ischemia and 7 min of reoxygenation. In each instance, this stimulus was followed by 90 min of simulated ischemia and 2 h of reoxygenation. In addition, the subthreshold preconditioned group had 20 min of previous ACE inhibitor treatment.

Results. Recovery of contractile function (percent of baseline) was 22 ± 1% (mean ± SEM) in the control group versus 61 ± 1% in the preconditioned group. The subthreshold preconditioned group and the ACE inhibitor-alone groups did not exhibit any protection; however, in combination, the protection was significant (71 ± 4% in the captopril group, 58 ± 8% in the lisinopril group, p < 0.005) compared with the control group. There was no significant difference between these values and recovery after the full preconditioning stimulus. Furthermore, Hoe 140, a specific bradykinin B₂ receptor antagonist, abolished the protection.

Conclusions. To our knowledge, these are the first results in human muscle to suggest that ACE inhibitors may augment ischemic preconditioning, possibly through B₂ receptor activation.

(J Am Coll Cardiol 1997;29:1599–606)