Jai Varma

Prediction of Hypertension Improvement After Stenting of Renal Artery Stenosis: Comparative Accuracy of Translesional Pressure Gradients, Intravascular Ultrasound, and Angiography

OBJECTIVES We investigated the comparative accuracy of renal translesional pressure gradients (TPG), intravascular ultrasound (IVUS), and angiographic parameters in predicting hypertension improvement after stenting of renal artery stenosis (RAS). BACKGROUND The degree of RAS that justifies stenting is unknown. METHODS In 62 patients with RAS, TPG (resting and hyperemic systolic gradient [HSG], fractional flow reserve, and mean gradient) were measured by a pressure guidewire; IVUS and angiographic parameters (minimum lumen area and diameter, area stenosis, and diameter stenosis) were measured by quantitative analyses. RESULTS The HSG had a larger area under the curve than most other parameters and an HSG >or=21 mm Hg had the highest sensitivity, specificity, and accuracy (82%, 84%, and 84%, respectively) in predicting hypertension improvement after stenting of RAS. The average IVUS area stenosis was markedly greater in RAS with an HSG >or=21 mm Hg versus <21 mm Hg (78% vs. 38%, respectively; p < 0.001). After stenting, hypertension improved in 84% of patients with an HSG >or=21 mm Hg (n = 36) versus 36% of patients with an HSG <21 mm Hg (n = 26) at 12 months, p < 0.01; the number of antihypertensive medications was significantly lower in patients with an HSG >or=21 mm Hg versus <21 mm Hg (2.30 +/- 0.90 vs. 3.40 +/- 0.50, respectively; p < 0.01). By multivariable analysis, HSG was the only independent predictor of hypertension improvement (odds ratio: 1.39; 95% confidence interval: 1.05 to 1.65; p = 0.013). CONCLUSIONS An HSG >or=21 mm Hg provided the highest accuracy in predicting hypertension improvement after stenting of RAS, suggesting that an HSG >or=21 mm Hg is indicative of significant RAS.

Postinfarct Cytokine Therapy Regenerates Cardiac Tissue and Improves Left Ventricular Function

We systematically investigated the comparative efficacy of three different cytokine regimens, administered after a reperfused myocardial infarction, in regenerating cardiac tissue and improving left ventricular (LV) function. Wild-type (WT) mice underwent a 30-minute coronary occlusion followed by reperfusion and received vehicle, granulocyte colony-stimulating factor (G-CSF)+Flt-3 ligand (FL), G-CSF+stem cell factor (SCF), or G-CSF alone starting 4 hours after reperfusion. In separate experiments, chimeric mice generated by reconstitution of radioablated WT mice with bone marrow from enhanced green fluorescent protein (EGFP) transgenic mice underwent identical protocols. Mice were euthanized 5 weeks later. Echocardiographically, LV function was improved in G-CSF+FL– and G-CSF+SCF–treated but not in G-CSF–treated mice, whereas LV end-diastolic dimensions were smaller in all three groups. Morphometrically, cytokine-treated hearts had smaller LV diameter and volume. Numerous EGFP-positive cardiomyocytes, capillaries, and arterioles were noted in the infarcted region in cytokine-treated chimeric mice treated with G-CSF+FL or G-CSF+SCF, but the numbers were much smaller in G-CSF–treated mice. G-CSF+FL therapy mobilized bone marrow–derived cells exhibiting increased expression of surface antigens (CD62L and CD11a) that facilitate homing. We conclude that postinfarct cytokine therapy with G-CSF+FL or G-CSF+SCF limits adverse LV remodeling and improves LV performance by promoting cardiac regeneration and probably also by exerting other beneficial actions unrelated to regeneration, and that G-CSF alone is less effective.

Recurrent aortic dissection in Marfan's syndrome: possible effects of anticoagulation.

&NA; Recent reports support the role of a valve‐sparing procedure in ascending aortic dissection in patients with Marfan’s syndrome. A 49‐year old woman with Marfan’s syndrome and prior aortic aneurysm repaired with a composite graft presented with sudden‐onset chest pain. Following an initial negative computed tomographic (CT) scan, a long dissection involving the descending thoracic and abdominal aorta was discovered on a repeat CT scan a few hours later. Symptoms improved gradually with optimal medical management and the patient was discharged home on anticoagulant therapy. Although no direct cause‐and‐effect relationship can be established, chronic anticoagulant therapy may accelerate the progression of recurrent dissection in these patients. A valve‐sparing procedure should be considered in eligible patients with Marfan’s syndrome who need operative correction to avoid possible future untoward effects of long‐term anticoagulant therapy.