W ELLIOTT

BACKGROUND: More than a decade ago, we found that a suboptimal medication regimen was the leading cause of resistant hypertension (RH) among patients referred to a tertiary care clinic. Since then, lower blood pressure (BP) goals have been recommended, suggesting that more patients may have RH. To assess whether the reasons for and treatment of RH have changed, we determined the frequency of various causes of resistance, the proportion of patients achieving goal BP, and the changes made in antihypertensive regimens. METHODS: The charts of all new patients seen at the RUSH University Hypertension Center between January 1, 1993, and November 1, 2001, were reviewed for strict criteria for RH: 1) physician referral for uncontrolled hypertension; 2) BP > or =140/90 mmHg despite use of three antihypertensive drugs; and 3) at least one follow-up visit. Patients were followed-up until goal BP was achieved on two consecutive visits or their last visit or until March 2002. RESULTS: Of 1281 patients, 141 met criteria for RH. A cause of resistance was found in 94% of cases, including the following: drug-related causes (58%); nonadherence (16%); psychological causes (9%); office resistance (ie, in-clinic BP readings that were higher than goal despite treatment with antihypertensive medications and despite normotensive BP outside of the clinic as demonstrated by 24-h ambulatory BP monitoring) (6%); and secondary hypertension (5%). Overall, 53% of patients had their BP controlled to <140/90 mmHg, largely from regimen optimization and intensification, proper use of diuretics, and on average 4.1 +/- 1 antihypertensive medications (3.7 +/- 0.9 on referral). CONCLUSIONS: These data are strikingly similar to those from our previous study of RH, in which a suboptimal medication regimen was the most common reason for resistance. Goal BP was most commonly achieved after optimizing the diuretic regimen and increasing the number of medications, suggesting that physicians should use these measures to attain the recommended lower BP goals If goal BP is not reached, referral to a clinical hypertension specialist may be appropriate.

An integrated approach, utilizing cine coronary angiography, the standard 12-lead and post-exercise electrocardiograms, and regional myocardial lactate metabolism, is presented for detection of regional myocardial ischemia in patients with coronary heart disease. The normal electrocardiogram was of no predictive value and was present with extensive coronary disease and myocardial production of lactate. The abnormal electrocardiogram gave an accurate indication of a portion, but not all zones of ischemia. Multiple electrocardiographic abnormalities were invariably associated with severe coronary artery disease, although in most patients many more coronary lesions were present than electrocardiographic abnormalities. The regional lactate pattern was very helpful in localizing myocardial ischemia and significant coronary artery lesions. Regional lactate abnormalities may have a great practical value in the selection of patients for myocardial revascularization surgery and in their postoperative evaluation.

The pathophysiology of cardiac pain in pure aortic stenosis has primarily been ascribed to an augmented left ventricular demand outstripping energy supply. This report provides evidence that not only is the energy demand increased but the supply in terms of coronary vascular reserve may be impaired, particularly in response to stress. Hemodynamic and coronary circulatory changes were studied in 18 patients with aortic stenosis during standard isoproterenol infusion. It was not possible to differentiate any patient with or without angina pectoris or patients with or without coronary artery disease on a basis of change in any measure of left ventricular dynamics. On the other hand, differences did occur in the mechanisms of energy delivery during isoproterenol stress: (1) In group A (aortic stenosis without angina or coronary artery disease), coronary flow increased normally, myocardial oxygen extraction decreased, and myocardial lactate production occurred in only one of seven patients. This suggested that energy supply was, generally, adequate to demand. (2) In group B (critical aortic stenosis with angina but no coronary disease), coronary flow rose insignificantly, myocardial oxygen extraction actually increased in three of five patients, and abnormal glycolysis occurred in all patients. This suggested that little or no reserve for increased coronary flow existed and that compensatory mechanisms had to be summoned. (3) In group C (aortic stenosis with angina and coronary artery disease), coronary flow rose normally, myocardial oxygen extraction decreased normally, but abnormal lactate metabolism occurred in most patients. This suggested adequate overall coronary reserve but evidence of regional ischemia.