Effect of abrupt mitral regurgitation after balloon valvuloplasty on myocardial load and performance

AbstractThe concept that mitral regurgitation masks myocardial dysfunction by reducing afterload and augmenting ejection performance has not been well established in humans. The effect of abruptly produced mitral regurgitation on left ventricular loading and performance was therefore evaluated in five patients who developed this complication after an otherwise successful percutaneous balloon mitral valvuloplasty. Mitral valve area by Gorlin formula calculated with forward flow increased from 0.92 ± 0.14 to 2.75 ± 0.82 cm2. Mean left atrial pressure did not decrease (19 ± 4 to 19 ± 6 mm Hg). The size of the left atrial Vwave relative to mean left atrial pressure (peak V— mean left atrial pressure) increased from 7 ± 4 to 19 ± 6 mm Hg. Angiographic mitral regurgitation increased from 0+ or 1 + to >3+ in each patient and regurgitant fraction increased from 0.23 ± 0.11 to 0.55 ± 0.99 (p < 0.01).End-diastolic volume increased modestly from 148 ± 15 to 159 ± 15 ml (p = NS). Heart rate increased from 54 ± 5 to 71 ± 8 heats/min (p < 0.05), which may have prevented further increases in preload by shortening the filling period. End-systolic stress decreased by 32% from 277 ± 34 to 188 ± 52 kdyn/cm2(p < 0.01) as a result of a 25% decrease in end-systolic pressure from 121 ± 8 to 91 ± 7 mm Hg and a 16% decrease in end-systolic volume from 67 ± 13 to 56 ± 8 ml (p = NS). Contractility estimated from the preload-corrected ejection fraction-afterload relation decreased in one of the five patients and did not increase in the others despite an increase in heart rate, possibly as a result of myocardial depression from the balloon procedure itself. Nevertheless, the decrease in end-systolic volume could not be attributed to a net increase in contractility. The result of the changes in loading was an increase in ejection fraction from 0.55 ± 0.05 to 0.65 ± 0.04 (p < 0.05).Thus, abruptly produced mitral regurgitation increases ejection performance by reducing afterload without increasing contractility. This should be taken into consideration when anticipating the results of valve replacement for acute or subacute mitral regurgitation

The Use of Flaps and Grafts in the Treatment of Urethral Stricture Disease

The use of various grafts and flaps plays a critical role in the successful surgical management of urethral stricture disease. A thorough comprehension of relevant anatomy and principles of tissue transfer techniques are essential to understanding the appropriate use of grafts or flaps to optimize outcomes. We briefly review these principles and discuss which technique may be best suited for a given anterior urethral stricture, depending on the location and length of the stricture, the presence or absence of an intact corpus spongiosum, and the availability of adequate and healthy penile skin

Evidence against a myocardial factor as the cause of left ventricular dilation in active rheumatic carditis

AbstractObjectives. The aim of this study was to determine whether left ventricular dilation and congestive heart failure in patients with acute rheumatic fever with carditis are accompanied by left ventricular contractile dysfunction.Background. Acute rheumatic fever with carditis involves both the myocardium and endocardium, with consequent valvular regurgitation. The relative contribution of volume overload induced by valvular regurgitation and myocardial dysfunction due to rheumatic myocarditis to the overall degree of left ventricular dilation and congestive heart failure in these patients is unknown.Methods. To investigate this, we evaluated 32 patients (15 male, 17 female, mean age 14 ± 3 years) with documented active carditis and congestive heart failure. All 32 patients were found to have significant isolated mitral regurgitation or combined mitral and aortic regurgitation. Echocardiographic analysis of left ventricular dimensions and systolic performance was performed before and after isolated mitral or combined mitral and aortic valve replacement and the results were compared with those in 19 control subjects matched for age, gender and body surface area.Results. Both preoperative left ventricular end-diastolic diameter and percent fractional shortening were significantly increased in patients compared with control subjects (57 ± 7 vs. 43 ± 3 mm, p < 0.001, and 38 ± 6% vs. 33 ± 1%, p < 0.001, respectively). After valve replacement, left ventricular end-diastolic diameter decreased significantly (57 ± 7 to 47 ± 6 mm, p < 0.001). Although percent fractional shortening decreased significantly postoperatively (38 ± 6% to 32 ± 6%, p < 0.001), the postoperative percent fractional shortening did not differ from that in control subjects (32 ± 6% vs. 33 ± 1%, p = NS).Conclusions. The results of this study indicate that left ventricular dilation and heart failure in patients with acute rheumatic carditis rarely occur in the absence of hemodynamically significant regurgitant valve lesions. Furthermore, rapid reduction in left ventricular dimensions and preservation of fractional shortening after isolated mitral or combined mitral and aortic valve replacement suggest that rheumatic carditis is not accompanied by any significant degree of myocardial contractile dysfunction

Excessive vasoconstriction in rheumatic mitral stenosis with modestly reduced ejection fraction

AbstractObjectives. The primary hypothesis examined was that underfilling due to inflow obstruction accounts for modestly depressed ejection performance in mitral stenosis, Having found little evidence to support this hypothesis, we sought to determine other factors that might differentiate patients with different levels of ejection performance.Methods. Ventricular load and performance were compared in two groups of patients before and immediately after successful balloon valvuloplasty that was not complicated by mitral regurgitation: those in whom prevalvuloplasty ejection fraction was ≥0.55 (group I, n = 10) and those in whom it was <0.55 (group II, n =11).Results. Before valvuloplasty, mitral valve area was less in group II (0.65 cm2) than in group I (0.84 cm2, p = 0.02), but end-diastolic pressure (12 vs. 12 mm Hg in group I), end-diastolic wall stress (46 vs. 44 kdynes/cm2in group I) and end-diastolic volume (152 vs. 150 ml in group I) were not less in group II, nor were these variables significantly reduced compared with those of a normal control group. In group II, end-systolic volume was larger (77 vs. 55 ml in group I, p = 0.001) and cardiac output was less (3.1 vs. 3.6 liters/min in group I, p = 0.03), possibly owing to higher systemic vascular resistance (2,438 vs. 1,921 dynes·s·cm−5in group I, p = 0.05) and end-systolic wall stress (273 vs. 226 kdynes/cm2in group I, p = 0.06), although mean arterial pressure in the two groups was similar (91 vs. 84 mm Hg in group I, p = 0.22). Group II patients also had higher values for pulmonary vascular resistance (712 vs. 269 dynes·s·cm−5in group I, p = 0.03) and mean pulmonary artery pressure (47 vs. 29 mm Hg in group I, p = 0.02) despite similar values for mean left atrial pressure (20 vs. 18 mm Hg in group I, p = 0.35). After valvuloplasty, mitral valve area increased by 2.5- and 3-fold, respeditely, in group I (to 2.1 cm2and group II (to 2.0 cm2). Modest increases in left ventricular end-diastolic pressure, end-diastolic stress and end-diastolic volume (+9%) after valvuloplasty were statistically significant only for group II. End-systolic wall stress did not decline in either group II (281 kdynes/cm2) or group I (230 kdynes/cm2), and ejection fraction failed to increase significantly (0.49 to 0.51 for group II and 0.62 to 0.61 for group I) after valvuloplasty. Contractile performance estimated with a preload-corrected ejection fraction-afterload relation was within or near normal limits in all 19 patients in whom it was assessed.Conclusions. Excessive vasoconstriction may account for the higher afterload, lower ejection performance and tower cardiac output observed in a subset of patients with mitral stenosis because contractile dysfunction could not be detected and left ventricular filling—which was not subnormal despite severe inflow obstruction—improved only modestly after valvuloplasty

Consensus guidelines for the use and interpretation of angiogenesis assays

The formation of new blood vessels, or angiogenesis, is a complex process that plays important roles in growth and development, tissue and organ regeneration, as well as numerous pathological conditions. Angiogenesis undergoes multiple discrete steps that can be individually evaluated and quantified by a large number of bioassays. These independent assessments hold advantages but also have limitations. This article describes in vivo, ex vivo, and in vitro bioassays that are available for the evaluation of angiogenesis and highlights critical aspects that are relevant for their execution and proper interpretation. As such, this collaborative work is the first edition of consensus guidelines on angiogenesis bioassays to serve for current and future reference