Quantitative evaluation of the amount of delayed myocardial enhancement as a predictor of systolic dysfunction.

30 patients with delayed contrast enhancement in patterns suggestive of myocardial infarctions were reviewed. Infarct mass was quantitatively measured using short axis images obtained in the delayed phase of gadopentetate administration. Left ventricular mass and ejection fraction were measured using short axis, steady state free precession images. A relationship is drawn between increased mass of infarction and decreased left ventricular ejection fraction. For each gram of infarct, there is a 0.5 % reduction in ejection fraction (EF = 50 - (0.48 x gm infarcted myocardium); r²= 0.49). For each % increase of infarcted myocardium, there is a 0.67 % reduction in ejection fraction (EF = 50 - (0.67 x percent of infarcted myocardium); r²= 0.39). Left ventricular ejection fraction correlates inversely with the mass of myocardium with delayed enhancement on cardiac MRI.

Anatomic and electrophysiologic relation between the coronary sinus and mitral annulus: implications for ablation of left-sided accessory pathways.

To determine whether precise left-sided accessory pathway localization is possible from the coronary sinus, electrocardiogram (ECG) characteristics from the coronary sinus pair demonstrating earliest activation via the accessory pathway were compared to simultaneous mitral annular ablation catheter ECGs at successful ablation sites in 48 patients. To define the coronary sinus-mitral annular relation, the coronary sinus to mitral annulus distance (D) was measured at sequential distances from the coronary sinus os in 10 cadaver hearts. Mitral annular ECGs demonstrated earliest activation via the accessory pathway more frequently than the earliest coronary sinus pair (p < 0.001), more frequent continuous electrical activity (p < 0.001), and more frequent accessory pathway potentials (p < 0.01). D was >10 mm at 20, 40, and 60 mm, respectively, from the coronary sinus os. Coronary sinus ECGs do not precisely localize left-sided accessory pathways, which may be due in part to an average anatomic separation of more than 10 mm between the coronary sinus and accessory pathways bridging the mitral annulus.

Acute effects of intraoperative multisite ventricular pacing on left ventricular function and activation/contraction sequence in patients with depressed ventricular function.

INTRODUCTION: We hypothesized that simultaneous right and left ventricular apical pacing would result in improvement in left ventricular function due to improved coordination of segmental ventricular contraction. Structural changes in ventricular muscle present in dilated cardiomyopathy compromise ventricular excitation and mechanical contraction. METHODS AND RESULTS: Eleven patients with depressed left ventricular function having cardiac surgery underwent epicardial multisite pacing with continuous transesophageal echocardiographic imaging. Quantitative measurement of percent fractional area change was performed, and segmental changes in contraction sequence resulting from simultaneous right and left ventricular pacing were assessed by application of phase analysis to recorded transesophageal images. There was no statistically significant difference between the paced QRS duration achieved with simultaneous right and left ventricular apical pacing and the native QRS duration (139+/-39 msec vs 106+/-18 msec, P = NS), but all other paced modes resulted in longer QRS durations. Percent fractional area change improved with simultaneous right and left ventricular apical pacing but not with other paced modes (41.5+/-11.9 vs 34.3+/-9.7, P < 0.01). Phase analysis demonstrated a resequencing of segmental left ventricular activation/contraction when compared to baseline ventricular activation. CONCLUSION: Simultaneous right and left ventricular apical pacing results in acute improvements in global ventricular performance in patients with depressed ventricular function. Improvements may result from pacing-induced global coordination through recruitment of left and right ventricular apical and septal segments critical to effective ventricular contraction.

Inappropriate sinus tachycardia. Diagnosis and treatment.

Inappropriate sinus tachycardia is characterized by consistently elevated heart rates and exaggerated responses to minimal physiologic activity. The syndrome of inappropriate sinus tachycardia is defined by the clinical presentation of palpitations and presyncope that commonly appear to be out of proportion to the severity of the tachycardia. The development of a potentially curative procedure for patients suffering from inappropriate sinus tachycardia has renewed interest in the treatment of such patients. Continued research directed at the pathophysiology of inappropriate sinus tachycardia and what the optimal end point for achieving adequate rate control by radiofrequency catheter ablation without the need for the implantation of a permanent pacemaker is required. The optimal treatment may be the use of drugs that specifically inhibit sinus node pacemaker current.

Evaluation of acute dual-chamber pacing with a range of atrioventricular delays on cardiac performance in refractory heart failure.

OBJECTIVES: This study evaluated how variations in atrioventricular (AV) delay affect hemodynamic function in patients with refractory heart failure being supported with intravenous inotropic and intravenous or oral inodilating agents. BACKGROUND: Although preliminary data have suggested that dual-chamber pacing with short AV delays may improve cardiac function in patients with heart failure, detailed Doppler and invasive hemodynamic assessment of patients with refractory New York Heart Association class IV heart failure has not been performed. METHODS: Nine patients with functional class IV clinical heart failure had Doppler assessment of transvalvular flow and right heart catheterization performed during pacing at AV delays of 200, 150, 100 and 50 to 75 ms. RESULTS: Systemic arterial, pulmonary artery, right atrial and pulmonary capillary wedge pressures, cardiac index, systemic and pulmonary vascular resistances, stroke volume index, left ventricular stroke work index (SWI) and arteriovenous oxygen content difference demonstrated no significant changes during dual-chamber pacing with AV delays of 200 to 50 to 75 ms. There were also no changes in the Doppler echocardiographic indexes of systolic or diastolic ventricular function. The study was designed with SWI as the outcome variable. Assuming a clinically significant change in the SWI of 5 g/min per m2, a type I error of 0.05 and the observed standard deviation from our study, the observed power of our study is 85% (type II error of 15%). CONCLUSIONS: Changes in AV delay between 200 and 50 ms during dual-chamber pacing do not significantly affect acute central hemodynamic data, including cardiac output and systolic or diastolic ventricular function in patients with severe refractory heart failure due to dilated cardiomyopathy.

Tachycardia-induced cardiomyopathy: a review of animal models and clinical studies.

The increasing prevalence of congestive heart failure has focused importance on the search for potentially reversible etiologies of cardiomyopathy. The concept that incessant or chronic tachycardias can lead to ventricular dysfunction that is reversible is supported by both animal models of chronic rapid pacing as well as human studies documenting improvement in ventricular function with tachycardia rate or rhythm control. Sustained rapid pacing in experimental animal models can produce severe biventricular systolic dysfunction. Hemodynamic changes occur as soon as 24 h after rapid pacing, with continued deterioration in ventricular function for up to 3 to 5 weeks, resulting in end-stage heart failure. The recovery from pacing-induced cardiomyopathy demonstrates that the myopathic process associated with rapid heart rates is largely reversible. Within 48 h after termination of pacing, hemodynamic variables approach control levels, and left ventricular ejection fraction shows significant recovery with subsequent normalization after 1 to 2 weeks. In humans, descriptions of reversal of cardiomyopathy with rate or rhythm control of incessant or chronic tachycardias have been reported with atrial tachycardias, accessory pathway reciprocating tachycardias, atrioventricular (AV) node reentry and atrial fibrillation (AF) with rapid ventricular responses. Control of AF rapid ventricular responses has been demonstrated to improve ventricular dysfunction with cardioversion to sinus rhythm, pharmacologic ventricular rate control and AV junction ablation and permanent ventricular pacing. The investigation of potential tachycardia-induced cardiomyopathy in patients with heart failure requires further prospective confirmation in larger numbers of patients, with study of mechanisms, patient groups affected and optimal therapies.

Asymmetric [14C]albumin transport across bullfrog alveolar epithelium.

Bullfrog lungs were prepared as planar sheets and bathed with Ringer solution in Ussing chambers. In the presence of a constant electrical gradient (20, 0, or -20 mV) across the tissue, 14C-labeled bovine serum albumin or inulin was instilled into the upstream reservoir and the rate of appearance of the tracer in the downstream reservoir was monitored. Two lungs from the same animal were used to determine any directional difference in tracer fluxes. An apparent permeability coefficient was estimated from a relationship between normalized downstream radioactivities and time. Results showed that the apparent permeability of albumin in the alveolar to pleural direction across the alveolar epithelial barrier is 2.3 X 10(-7) cm/s, significantly greater (P less than 0.0005) than that in the pleural to alveolar direction (5.3 X 10(-8) cm/s) when the tissue was short circuited. Permeability of inulin, on the other hand, did not show any directional dependence and averaged 3.1 X 10(-8) cm/s in both directions. There was no effect on radiotracer fluxes permeabilities of different electrical gradients across the tissue. Gel electrophoretograms and corresponding radiochromatograms suggest that the large and asymmetric isotope fluxes are not primarily due to digestion or degradation of labeled molecules. Inulin appears to traverse the alveolar epithelial barrier by simple diffusion through hydrated paracellular pathways. On the other hand, [14C]albumin crosses the alveolar epithelium more rapidly than would be expected by simple diffusion. These asymmetric and large tracer fluxes suggest that a specialized mechanism is present in alveolar epithelium that may be capable of helping to remove albumin from the alveolar space.