Acute and late outcome after use of 2.5-mm intracoronary stents in small (< 2.5 mm) coronary arteries.

We describe the high-pressure deployment of 2.5-mm stents in small (< 2.5 mm) coronary vessels. Forty-three lesions in 40 patients were treated. The mean reference vessel diameter was 2.3 +/- 0.2 mm. The mean % luminal stenosis was 90 +/- 9. The mean lesion length was 11. 7 +/- 9.1 mm. Sixteen lesions were pretreated with rotational atherectomy, and the remainder with PTCA. The rate of successful stent deployment was 41/43 (95%). The mean postintervention % stenosis was -1 +/- 10. There were no in-hospital deaths or procedure-related Q-wave MI. The patients were followed for a mean of 18 months. Eight patients (or 21%) developed recurrent chest pain and/or angiographically proven restenosis. One patient (3%) developed intermediate restenosis. Twenty-nine patients (or 76%) either remain symptom-free or have patent target sites on repeat angiography. It appears that reasonable acute and long-term results can be achieved with 2.5-mm stents in small coronary arteries using high-pressure deployment techniques. Cathet. Cardiovasc. Intervent. 49:121-126, 2000.

Improved technique for use of half-stents remounted on a stent delivery system.

The use of half-length intracoronary Johnson & Johnson stents has been described in a number of settings. Half-stents are useful for very short lesions, avoidance of bifurcations or side-branches, ostial stenosis, covering gaps between adjacent stents, and for dissection adjacent to stents caused by postdilatation. Previously described methods for use of half-stents have involved bare stents, or significant manipulation of either the stent or the delivery sheath for remounted half-stents. We describe a method for half-stent preparation and delivery that does not involve distortion of the stent or the delivery sheath. The risk of stent loss, as can occur with bare stents, is diminished. The geometry of the stent is preserved since it is not expanded and then recrimped, and the end of the delivery sheath is not flared or distorted, which may interfere with stent delivery.

Catecholamine response to chronic ANG II infusion and its role in myocyte and coronary vascular damage.

Acute elevations in circulating angiotensin II (ANG II) are known to increase circulating norepinephrine (NE) levels. However, the time course of catecholamine release relative to chronic ANG II infusion is not known. Furthermore, it is unknown if this ANG II-induced catecholamine release is ANG II type 1 (AT1) receptor mediated or whether the increase in serum catecholamines is responsible for the myocyte and coronary vascular damage seen within the first 3 days of chronic ANG II infusion. Therefore, we examined the influence of chronic ANG II stimulation on serum catecholamine levels with and without AT1 blockade and the effect of beta-blockade on ANG II-induced myocyte and coronary vascular damage. The results indicate that NE release is AT1 mediated, but NE is not significantly elevated until day 4 of ANG II infusion after which it remains elevated. beta-Blockade prevented most ANG II-related myocyte necrosis and coronary vascular damage. Therefore, myocyte and coronary vascular damage do not appear to be related to increased serum NE levels, but instead may be due to the release of neural catecholamines within the heart.

Prevention of angiotensin II induced myocyte necrosis and coronary vascular damage by lisinopril and losartan in the rat.

OBJECTIVE: The aims were to determine: (1) if angiotensin converting enzyme (ACE) inhibition and angiotensin II receptor blockade can prevent angiotensin II induced coronary vascular damage; (2) if the cardioprotective properties of ACE inhibition are dose dependent; and (3) if the cardioprotective properties of ACE inhibition are independent of its ability to prevent the conversion of angiotensin I to angiotensin II. METHODS: Control rats and rats with either renovascular hypertension or continuous angiotensin II infusion (150 ng.min-1) for 14 d were subdivided into nine groups as follows: unoperated and untreated controls (n = 5); untreated renovascular hypertension (n = 8); untreated angiotensin II (n = 9); a renovascular hypertension group receiving one of the following doses of lisinopril 20 (n = 8), 2.5 (n = 4), and 0.6 (n = 6) mg.kg-1.d-1; a renovascular hypertension group receiving losartan (7.5 mg.d-1, n = 4); and an angiotensin II group receiving either the high dose of lisinopril (n = 6) or losartan (n = 4). Treatment was started one day before initiation of renovascular hypertension and angiotensin II infusion and continued throughout the study period. The number and size of necrotic areas and numbers of damaged coronary vessels were determined in sections of right and left ventricular tissue. RESULTS: Both coronary vascular injury and myocyte injury induced by angiotensin II were prevented by losartan. In renovascular hypertension, the lowest dose of lisinopril prevented vascular and attenuated myocyte damage but to a lesser degree than the higher doses. The cardioprotective ability of ACE inhibition is primarily the result of its ability to prevent the conversion of angiotensin I to angiotensin II. CONCLUSIONS: Angiotensin II related cardiomyocyte necrosis and coronary vascular damage are angiotensin type 1 receptor mediated and completely preventable with the receptor antagonist losartan. The ability of ACE inhibition to prevent this damage is dose dependent and primarily related to the degree to which the inhibitor can prevent the conversion of angiotensin I to angiotensin II.

Angiotensin II (AII)-induced myocyte necrosis: role of the AII receptor.

Pathophysiologic levels of angiotensin II (AII) produce myocyte necrosis. We investigated whether the cardiotoxic effects of AII are mediated through the AII type I receptor (AT1). Seven groups (4-6 rats/group) were given AII (150 ng/min) alone or in combination with the AT1 antagonist losartan (7.5 mg/day). Groups were as follows: A1, A4, and L1 received AII for 2 days; A2 and L2 received AII for 9 days; and A3 and L3 received AII for 2 days and again for 2 days 5 days later. Groups L1, L2, and L3 also received losartan 2 days before and throughout the AII infusion period. All rats except those in group A4 were killed at the end of their respective infusion periods (group A4 rats were killed 7 days after infusion). Group A1 had multifocal areas of recent myocyte injury. Groups A2 and A4 had multifocal scars and only a few new areas of myocyte damage. Group A3, in addition to scar formation, had de novo areas of necrosis. There was no evidence of myocyte necrosis in groups L1, L2, and L3. Thus, AII-related myocyte necrosis is receptor mediated. Moreover, a chronic increase in AII appears to cause cardioprotective downregulation of the AT1 receptor.

Myocardial collagen and its functional role.

Even though normally present in relatively small amounts, myocardial collagen strongly influences ventricular diastolic function. Removal of less than half of the normal amount results in a dilated ventricle with increased compliance. In contrast, an abnormal increase in collagen concentration results in a stiffer myocardium and ventricular diastolic dysfunction.