OBJECTIVES The purpose of this study was to assess whether the newer stent delivery systems provide a stented lumen cross-sectional area (CSA) that is equal to the delivery balloon nominal dimensions.BACKGROUND First generation stents were often not adequately expanded with their delivery system and frequently required higher pressure or a larger balloon after deployment. Newer stents were designed to optimize expansion with noncompliant, high-pressure balloons provided as the delivery systems.METHODS Intravascular ultrasound (IVUS) was used to evaluate 38 stents in 32 patients after deployment at 14 to 16 atm with their delivery balloon system. Minimum stent lumen CSA and stent minimum lumen diameter (MLD) were measured by IVUS imaging. The manufacturer's expected stent diameter was defined as the balloon diameter measured by the company at the maximum pressure used. The manufacturer's expected stent area was calculated based on the manufacturer's expected stent diameter.RESULTS The MLD (2.5 +/- 0.5 mm) and minimum stent CSA (6.0 +/- 1.7 mm(2)) by, IVUS were significantly smaller than the manufacturer's expected stent diameter (3.5 +/- 0.4 mm) and area (9.5 +/- 1.9 MM2) (p < 0.0001, respectively). The mean MLD by IVUS was 72 +/- 8% of the expected stent diameter, and the mean minimum stent CSA by IVUS was 62 +/- 10% of the expected stent area.CONCLUSIONS Despite moderately high-pressure inflations, the mean minimum stent CSA actually achieved was, on average, only 62% of the manufacturer's expected stent area. To optimize stent deployment, these IVUS observations should be considered during coronary artery stenting. (C) 2001 by the American College of Cardiology.

A considerably large number of ECGs of pediatric patients had small notches and slurs on QRS complexes. By sampling these ECGs at higher rates, namely 4 KHz, it was shown that the higher rate data accurately reconstructed the notches and slurs on the QRS complex which were occasionally missed or distorted when the sampling rate was 250 Hz.When using the sampling rate of 250 Hz, it was observed that the reduction of the peak-to-peak amplitude of a QRS complex exceeded 0.1 mV in nearly 30 percent of tested cases, even if the ECG did not contain unwanted noise signals. Moreover, if there is relatively more noise in children's ECGs, one should reduce noise in such data in order to prevent measurement errors in the succeeding steps of the computer program. In such circumstances, the higher sampling rate would be preferable since filtering techniques which are used to reduce noise may considerably affect the estimation of the onset, offset and amplitude of the intrinsic ECG signals if the sampling rate is low.The reduction of the price of computers and their peripheral devices may facilitate the adoption of the higher sampling rate. From these considerations it was concluded that the use of the higher sampling rate might be both practical and an effective measure to enhance the diagnostic performance of the computer ECG systems.

Many investigators have reported the use of various permanent pacemaking modes in the long‐term management of patients with recurrent ventricular tachycardia.1–9 The three general types of antitachycardic pacemakers are; (1) underdrive; (2) burst; and (3) scanning pacemakers, Such devices have been activated externally or have had automatic activation. Each antitachycardic pacemaking modality has known technical and physiologic limitations. A serious limitation of dual‐demand underdrive pacemakers is that they are usually successful only for tachycardias with a rate below 160 bpm becsuse a random stimulus is needed for conversion.7 Therefore, this modality is seldom useful in patients with symptomatic sustained ventricular tachycardia in which rates are generally greater than 160 bpm and/ or hemodynamic compromise occurs rapidly. Although others have reported the successful use of burst pacemakers in the control of ventricular tachycardia, this technique may cause acceleration of ventricular tachycardia and induction of ventricular fibrillation.1.3.5–9 Programmable automatic scanning pacemakers have been used successfully to treat paroxysmal supraventricular tachycardia10 and have been used recently in combination with antiarrhythmic agents to control ventricular tachycardia.11 This report outlines the use of an automatic scanning pacemaker alone for the treatment of symptomatic ventricular tachycardia in a patient who was unable to tolerate conventional antiarrhythmic medications.

Uninephrectomized, saline-fed male Sprague-Dawley rats were given DOCA 5 mg per week alone or together with progesterone 20 mg per week for 6 weeks (phase I). Subsequently, the doses of DOCA and progesterone were doubled and the rats were studied for an additional 6 wk (phase II). Progesterone prevented DOCA-induced hypertension during phase I. Phase II blood pressures were higher in DOCA-progesterone-treated animals than in controls, but remained lower than in animals treated with DOCA alone. At the end of phase II the animals were killed, and blood samples and skeletal muscle samples were taken for analysis of electrolyte content. DOCA-treated animals were found to have an increased rate of potassium excretion, an increase in muscle sodium concentration, and a decrease in muscle potassium concentration compared to the controls. Progesterone treatment significantly blunted the DOCA-induced changes in muscle electrolyte concentrations and increased the rate of sodium excretion. No hypotensive effect was observed when progesterone in doses similar to those of phase I was administered to spontaneously hypertensive rats. Thus, in experimental mineralocorticoid hypertension, the hypotensive effect of progesterone appears to correlate closely with its mineralocorticoid antagonistic properties.

Progesterone increases urinary sodium excretion at least in part by competition for renal mineralocorticoid receptors. In contrast, synthetic progestagens do not increase sodium excretion or even cause a slight sodium retention. We therefore compared the ability of progesterone and 12 progesterone like compounds to displace [3H]aldosterone from binding at cytoplasmic mineralocorticoid receptors in rat kidney. All synthetic progesteronelike steroids were less active than progesterone in competing with [3H]aldosterone for the receptor binding: progesterone 100%, 11 beta-OH progesterone 50%, 17 alpha OH-progesterone 24% and 16 alpha-methyl-progesterone 3%. Derivates of 17 alpha OH-progesterone (medrogestone 5%, dydrogestone 4%, medroxy progesterone-acetate 2% and chlormadinone-acetate 0.5%) were more potent than 19-nor-testosterone derivates: ethisterone 1%, norethisterone less than 1%, norethindrone less than 1%, norethyl-nodrel less than 1%, and ethynodiol-diacetate less than 1%. The decreased affinity of synthetic progestins for mineralocorticoid receptors explains in part the lack of natriuretic activity of these compounds.

The ability of progesterone to increase sodium excretion only in the presence of active mineralocorticoids has led to the suggestion that progesterone antagonizes mineralocorticoid action at the renal tubular level. We have examined the effects of progesterone and aldosterone on sodium and potassium excretion in adrenalectomized rats and have compared these results with the ability of progesterone to inhibit the binding of aldosterone to cytoplasmic and nuclear mineralocorticoid receptors. The administration of aldosterone to saline-loaded, adrenalectomized male rats resulted in a dose-dependent fall in the urinary sodium to potassium ratio with a near maximum effect produced by 1 μg aldosterone. Progesterone alone in doses of 10, 100, and 1000 μg had no significant effect on the sodium to potassium ratio, but when administered simultaneously with 1 μg aldosterone, the same concentrations of progesterone inhibited the effect of aldosterone in a dose-dependent manner; 1 mg progesterone completely blocked t...

ACTH alpha 1-24 was infused at incremental rates of 12.5-200 mIU/30 min in dexamethasone-suppressed hypertensive patients on a regular sodium diet. The plasma aldosterone response to this stimulus in 8 patients with hyperaldosteronism due to an adrenal aldenoma and 11 with adrenal hyperplasia was significantly greater at all infusion rates (P less than 0.05) when compared with the response in 6 normal subjects on a similar diet. This responsiveness to ACTH in the patients with primary hyperaldosteronism was similar to that of the normal subjects on a low sodium diet. Twelve patients with low renin and 6 patients with normal renin essential hypertension were similarly studied. There was no significant difference in the median aldosterone response between these 2 groups and the normal subjects on a normal diet, but the response was significantly lower compared with that in patients with primary hyperaldosteronism. These data show that patients with hyperaldosteronism from an adrenal adenoma or hyperplasia have a consistent and exaggerated response to ACTH. The hyper-responsiveness is not apparently shared by the majority of patients with low renin essential hypertension and does not support the concept that this group is an intermediate form of primary aldosteronism. Individual patients within this group, however, may have such a response and might be identified by this type of testing.