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Renal artery stenting may improve blood pressure (BP) and renal function in resistant hypertension patients; however, benefit may differ depending on the degree of renal dysfunction. The authors analyzed 67 consecutive patients receiving stenting for obstructive renal artery disease between 2002 and 2005. Patients were categorized as normal or mildly impaired according to estimated glomerular filtration rate (eGFR) (or =60 mL/min/1.73 m(2)), moderately impaired (eGFR 30 to 59 mL/min/1.73 m(2)), and severely impaired (eGFR30 mL/min/1.73 m(2)). In patients with eGFRor =60, systolic BP did not significantly improve from baseline. However, in patients with an eGFR between 30 and 59 mL/min/1.73 m(2), systolic BP decreased by 12 mm Hg at 6 months (P=.02) and 14 mm Hg at 12 months (P=.01). Greater benefit was observed in patients with eGFR30 mL/min/1.73 m(2), with a 16 mm Hg (P=.10) and 21 mm Hg (P=.02) decrease at 6 and 12 months, respectively. Renal function was stable across all groups. Renal artery stenting reduced BP and produced greatest benefit in patients with baseline impaired renal function.

Distal embolic protection (DEP) may prevent embolization of atherosclerotic debris during renal artery stenting. The authors retrospectively identified 48 hypertensive patients with chronic kidney disease (CKD) who underwent renal artery stenting between 2002 and 2005 and compared stenting alone (n=17) to stenting/DEP (n=31). Blood pressure (BP) and estimated glomerular filtration rate (eGFR) (mL/min/1.73m(2)) at baseline at 6 and 12 months were compared. Overall, eGFR improved by 4.7 (P=.005) at 6 months and 3.8 (P=.003) at 12 months compared with baseline. Comparing stent to stent/DEP patients, eGFR improvement did not differ at 6 months (7.6 vs 2.9; P=.15) or at 12 months (4.4 vs 3.5; P=.74). Systolic BP reduction was similar between stent and stent/DEP patients at 6 months (−9 vs −14 mm Hg; P=.59) and at 12 months (−18 vs −16 mm Hg; P=.89). Renal artery stenting improved eGFR and systolic BP in patients with hypertension and CKD; however, DEP did not enhance these effects.

The epidemic of obesity in the United States and around the world is intensifying in severity and scope and has been implicated as an underlying mechanism in systemic hypertension. Obese hypertensive individuals characteristically exhibit volume congestion, relative elevation in heart rate, and high cardiac output with concomitant activation of the renin-angiotensin-aldosterone system. When the metabolic syndrome is present, insulin resistance and hyperinsulinemia may contribute to hypertension through diverse mechanisms. Blood pressure can be lowered when weight control measures are successful, using, for example, caloric restriction, aerobic exercise, weight loss drugs, or bariatric surgery. A major clinical challenge resides in converting short-term weight reduction into a sustained benefit. Pharmacotherapy for the obese hypertensive patient may require multiple agents, with an optimal regimen consisting of inhibitors of the renin-angiotensin-aldosterone system, thiazide diuretics, beta-blockers, and calcium channel blockers if needed to attain contemporary blood pressure treatment goals.

Left ventricular diastolic properties are important markers of pump function and are frequently abnormal when myocardial insults alter tissue structure. Alterations can be limited to the early diastolic phase (early active relaxation) or to late diastolic filling (late ventricular compliance), but more often involve regulation of both phases of diastole. In asymptomatic patients with arterial hypertension, left ventricular relaxation is often prolonged, independently, at least in part, of cardiac loading conditions and left ventricular geometry, but this abnormality is associated with early signs of systolic dysfunction. Uncontrolled hypertension, diabetes, and obesity are most often associated with ischemic heart disease and impaired diastolic function. Reducing blood pressure with antihypertension therapy will reduce myocardial afterload, regress LVH, and improve systolic and diastolic function. In patients with symptoms of CHF with a normal ejection fraction, however, changes in therapy may be indicated. Greater emphasis should be placed on using medications that decrease myocardial load, but also reduce the effects of neurohormonal activation.