Coronary vasomotion after percutaneous transluminal coronary angioplasty depends on the severity of the culprit lesion.

OBJECTIVES: This study sought to evaluate coronary vasomotor response to percutaneous transluminal coronary angioplasty (PTCA) and its influence on proximal and distal vessel diameters with regard to stenosis severity and coronary blood flow. BACKGROUND: Coronary vasoconstriction of the distal vessel segment has been reported after PTCA. This vasoconstrictive effect was thought to be due to balloon-induced injury of the vessel wall, with release of local vasoconstrictors or stimulation of the sympathetic system with release of catecholamines, or both. METHODS: Thirty-nine patients were prospectively studied before and after PTCA. Patients were classified into two groups according to the severity of the culprit lesion: group 1 = > or = 70% to < or = 85% diameter stenosis (n = 23); and group 2 = > 85% to < or = 95% diameter stenosis (n = 16). The coronary vessel diameter of the proximal and distal vessel segments as well as the minimal lumen diameter were determined by quantitative coronary angiography. In a subgroup of 16 patients, basal and maximal coronary flow velocity was measured before and after PTCA with the Doppler FloWire system. RESULTS: The groups were comparable with regard to age, gender, serum cholesterol levels and medical therapy. The proximal vessel segment remained unchanged after PTCA in group 1 ([mean +/- SD] 0.9 +/- 3.5%, p = 0.8) but showed vasodilation in group 2 (+13.7 +/- 3.6%, p < 0.05). However, the distal segment showed vasoconstriction in group 1 (-6.7 +/- 2.0%, p < 0.01) and vasodilation in group 2 (+31 +/- 8.0%, p < 0.01). A significant correlation was found between the change in distal vessel diameter after PTCA and stenosis severity (r = 0.61, p < 0.0001). Changes in blood flow were directly correlated to stenosis severity (r = 0.85, p < 0.002); that is, rest flow increased after PTCA in narrow lesions but remained unchanged in moderate lesions. The diameter changes in the distal vessel segment after PTCA were significantly related to flow changes (r = 0.90, p < 0.0001). Coronary distending pressure of the distal vessel segment increased significantly in both groups; however, this increase was significantly greater in group 2 than in group 1 (55 +/- 4 vs. 14 +/- 3 mm Hg, p < 0.0001). CONCLUSIONS: Coronary vasomotion of the proximal and distal vessel segments after PTCA depends on the severity of the culprit lesion; that is, vasoconstriction of the distal segment is found in patients with moderate lesions and vasodilation in those with severe lesions. Thus, vasomotion of the post-stenotic vessel segment depends on the severity of the culprit lesion and is influenced by changes in coronary flow or distending pressure, or both.

Enhanced alpha-adrenoreceptor-mediated vasoconstriction in essential hypertension.

Forearm blood flow (FAF) has been determined using venous occlusion plethysmography in 24 patients with essential hypertension (EHT) and in 16 age-matched normotensive subjects (NT) under basal resting conditions, following nonspecific vasodilatation with sodium nitroprusside and after intraarterial infusion of the postjunctional alpha-blocking drug, prazosin. Under basal conditions, FAF was significantly higher in EHT than in NT. Infusion of sodium nitroprusside produced a similar absolute increase in FAF in both groups, whereas postjunctional alpha-blockade with prazosin led to a significantly greater increase in FAF in EHT than in NT. A positive correlation was found between plasma epinephrine concentration and prazosin-induced FAF in EHT but not in NT. These results suggest an enhanced postjunctional alpha-adrenoreceptor-mediated vasoconstrictor component in established EHT.

Enhanced vasodilatation in essential hypertension by calcium channel blockade with verapamil.

The dependency of arteriolar tone on calcium influx was studied in 11 patients with essential hypertension (EH) and compared to 11 age-matched normotensive subjects (NT) by measuring the forearm blood flow response to intraarterial infusion of the calcium channel blocker verapamil (Verap) and the non-specific vasodilator sodium nitroprusside (Nip) using venous occlusion plethysmography. Verap in incremental dosages from 1 to 75 micrograms/100 ml forearm tissue induced a greater increase in forearm blood flow ( delta FAF) in EH then in NT, whereas there was no significant difference in delta FAF following Nip 1,2 micrograms/100 ml tissue. Delta FAF to Verap as adjusted for delta FAF to Nip was still greater in EH than in NT. Delta FAF to all dosages of Verap correlated positively with basal plasma epinephrine concentration in EH. At the two highest dosages of Verap, systemic blood pressure fell in EH, and the Verap-induced vasodilator (as adjusted for the response to Nip) correlated negatively to plasma renin activity or plasma angiotensin II concentration. These findings support the concept of an increased dependency of arteriolar tone on calcium influx in EH, which is related to the activity of the sympathetic nervous system. This association may be due to a common underlying derangement in transmembranous ionic fluxes in smooth muscle cells and sympathetic neurons in EH.

Antihypertensive and renal effects of captopril in relation to renin activity and bradykinin-induced vasodilation.

The effect of captopril on blood pressure and renal hemodynamics in relation to plasma renin activity (PRA) was assessed together with the vasodilator responses to brachial artery infusions of bradykinin (BK) and sodium nitroprusside (NP) before and after 4 wk of therapy with doses of up to 450 mg/day in patients with essential hypertension. The average blood pressure reduction of captopril was from 174.4/110.6 to 155.3/96.6 mm Hg (n = 12, P less than 0.001) without increases in heart rate or body weight. It was effective in the eight patients with normal renin, but showed little effect in the four with a low renin. There was a correlation between the changes in blood pressure after captopril and the pretreatment PRA (r = -0.82, P less than 0.01 for mean pressure). Brachial artery infusions of BK and NP induced dose-dependent rises in forearm blood flow (FBF), but this was not related to the captopril blood pressure-lowering effect. Repeat measurements during captopril therapy showed a shift to the left of the BK/FBF, but not of the NP/FBF, dose-response curve, indicating effective vascular kininase II inhibition. Captopril decreased renal vascular resistance. Our data are compatible with the view that captopril's antihypertensive action mainly involves blockade of the renin-angiotensin-aldosterone system and not cumulation of BK. The favorable effects on renal hemodynamics and the lack of tachycardia and volume retention after captopril make it a valuable drug for the treatment of hypertension.

Echocardiography in the evaluation of systolic murmurs of unknown cause.

PURPOSE: Systolic murmurs are common, and it is important to know whether physical examination can reliably determine their cause. Therefore, we prospectively assessed the diagnostic accuracy of a cardiac examination in patients without previous echocardiography who were referred for evaluation of a systolic murmur. SUBJECTS AND METHODS: In 100 consecutive adults (mean [+/- SD] age of 58 +/- 22 years) who were referred for a systolic murmur of unknown cause, the diagnostic accuracy of the cardiac examination by cardiologists (without provision of clinical history, electrocardiogram, or chest radiograph) was compared with the results of echocardiography. RESULTS: The echocardiographic findings included a normal examination (functional murmur) in 21 patients, aortic stenosis in 29 patients, mitral regurgitation in 30 patients, left or right intraventricular pressure gradient in 11 patients, mitral valve prolapse in 11 patients, ventricular septal defect in 4 patients, hypertrophic obstructive cardiomyopathy in 3 patients, and associated aortic regurgitation in 28 patients. In 28 (35%) of the 79 patients with organic heart disease, more than one abnormality was found; combined aortic and mitral valve disease was the most frequent combination (n = 22). The sensitivity of the cardiac examination was acceptable for detecting ventricular septal defect (100% [4 of 4]), isolated mitral regurgitation (88% [26 of 36]), aortic stenosis (71% [21 of 29]), and a functional murmur (67% [14 of 21]), but not for intraventricular pressure gradients (18% [2 of 11]), aortic regurgitation (21% [6 of 28]), combined aortic and mitral valve disease (55% [6 of 11]), and mitral valve prolapse (55% [12 of 22]). In 6 patients, the degree of aortic stenosis was misjudged on the clinical examination, mainly because of a severely diminished left ventricular ejection fraction. Significant heart disease was missed completely in only 2 patients. CONCLUSION: In adults with a systolic murmur of unknown cause, a functional murmur can usually be distinguished from an organic murmur. However, the ability of the cardiac examination to assess the exact cause of the murmur is limited, especially if more than one lesion is present. Thus, echocardiography should be performed in patients with systolic murmurs of unknown cause who are suspected of having significant heart disease.

Isradipine improves endothelium-dependent vasodilation in normotensive coronary artery disease patients with hypercholesterolemia.

OBJECTIVE: The dihydropyridine calcium antagonist isradipine has anti-atherosclerotic effects in animals and improves endothelium-mediated nitric oxide (NO)-dependent vasodilation in vitro. As improved endothelial function may be beneficial we investigated its effects in patients with a high likelihood of endothelial dysfunction. DESIGN: Thirty patients (two female, age 55.4 +/- 10.5 years) with known coronary artery disease and elevated (> 6 mmol/l) total cholesterol (cholesterol: mean 6.7 +/- 0.78 mmol/l) or a cholesterol/high density lipoproteins (HDL) ratio of > 5 not on lipid lowering therapy, participated in the study. Endothelial vasodilator function was assessed before and after double-blind, randomized administration of isradipine 5 mg/day or placebo for 3 months. METHODS: Endothelial function was assessed as forearm blood flow (FBF, venous occlusion plethysmography) responses to graded brachial artery infusions of acetylcholine (Ach), to the NO-synthase blocker NG-monomethyl-L-arginine (L-NMMA) and to the endothelium-independent vasodilator sodium nitroprusside (SNP). Blood pressure was measured either directly from the brachial arterial or by sphygmomanometer during clinic visits. RESULTS: Blood pressure was unchanged in both groups after 3 months (isradipine: 88.8 versus 92.1 mmHg; placebo: 81.0 versus 82.5 mmHg; NS) but cholesterol levels decreased similarly in both groups (isradipine: 6.7 versus 6.1 mmol/l, NS; placebo: 6.6 versus 5.9 mmol/l, P< 0.05). The vasodilator response to SNP and the decrease in FBF in response to blockade of NO synthesis by L-NMMA were unchanged in both groups. However, isradipine, but not placebo, enhanced the NO-dependent vasodilator response to Ach (P < 0.05). CONCLUSION: Isradipine improves acetylcholine-mediated vasodilation in hypercholesterolemic patients independent of changes in lipids or blood pressure.

Relation of cyclosporine blood levels to adverse effects on lipoproteins.

Hyperlipidemia is common in renal allograft recipients. To elucidate the role of cyclosporine in posttransplant hyperlipidemia, we measured lipids, lipoprotein lipids, and apolipoproteins of thirty-five renal allograft recipients and evaluated their relation to trough cyclosporine blood levels. All patients were on a triple immunosuppressive regimen with equal doses of prednisone and azathioprine, and had stable graft function. Cyclosporine blood levels were significantly correlated to total plasma cholesterol (P = 0.028), low-density lipoprotein cholesterol (P = 0.022), apolipoprotein B (P = 0.017), and the cholesterol/high-density lipoprotein cholesterol ratio (P < 0.002), but not to plasma triglycerides. Significant inverse correlations were found between cyclosporine blood levels and high-density lipoprotein cholesterol (P = 0.034), high-density lipoprotein3 cholesterol (P = 0.025), and apolipoprotein A-1 (P = 0.047), but not high-density lipoprotein2 cholesterol. The independent relation of cyclosporine blood levels to each of the measured lipid parameters was investigated by a stepwise regression model including age, body mass index, interval from transplantation, diabetes mellitus, plasma creatinine, and intake of diuretics and beta-blockers. After correction for these 7 variables, cyclosporine blood levels remained significantly associated with high-density lipoprotein cholesterol, high-density lipoprotein3 cholesterol, apolipoprotein A-1, apolipoprotein B, low-density lipoprotein cholesterol, and the cholesterol/high-density lipoprotein cholesterol ratio. These data suggest that cyclosporine causes atherogenic dyslipidemia.

Relation of the level of high-density lipoprotein subfractions to the presence and extent of coronary artery disease.

Plasma lipid profiles, including high-density lipoprotein (HDL) subfractions HDL2 and HDL3, were obtained in 115 men undergoing coronary angiography to assess the relation of lipid levels to coronary artery disease (CAD). CAD was present in 87 patients (76%) and absent in 28 (24%). The largest difference between the 2 groups were observed for HDL2 cholesterol, with a mean of 0.13 mmol/liter (5 mg/dl) in patients with CAD compared with 0.25 mmol/liter (10 mg/dl) in those without CAD (p less than 0.005). Smaller differences were found for HDL3 (1.02 mmol/liter [39 mg/dl] vs 1.19 mmol/liter [46 mg/dl]; p less than 0.005) and HDL (1.15 vs 1.42 mmol/liter [45 vs 55 mg/dl]; p less than 0.001) cholesterol, and apolipoprotein A-1 (1.37 vs 1.50 g/liter; p less than 0.01) and plasma triglycerides (1.79 vs 1.38 mmol/liter [159 vs 122 mg/dl]; p less than 0.05). No significant difference was found for plasma and low-density lipoprotein cholesterol, and apolipoprotein B levels. Simple regression analysis revealed that the most powerful independent variable associated with the extent of CAD was HDL2 cholesterol (Spearman rho = 0.311; p less than 0.001). Stepwise multiple regression analysis proved HDL2 cholesterol and age to be the strongest predictors of extent of CAD. The level of HDL2 cholesterol was reasonably well correlated with HDL cholesterol (r2 = 0.6; p less than 0.0001), but less so with plasma apolipoprotein A-1 (r2 = 0.4; p less than 0.0001). The data add to the growing body of information demonstrating an important association of HDL (and more specifically HDL2) with CAD in men.

Pulmonary hypertension five years after left pneumonectomy for adenoid cystic carcinoma.

We report the findings in a patient with shortness of breath due to pulmonary hypertension five years after left pneumonectomy. Mediastinal recurrence of an incompletely resected and slowly growing adenoid cystic carcinoma of the left main bronchus had encased the right main pulmonary artery.

Ventricular fibrillation in a patient with exercise-induced anaphylaxis, normal coronary arteries, and a positive ergonovine test.

Exercise-induced anaphylaxis (EIA) is a rare form of physical allergy. Although histamine release is a feature of EIA, and histamine provocation of coronary spasm has been described, serious cardiac arrhythmias in EIA have not been reported. Exercise-induced anaphylaxis was diagnosed in a survivor of out-of-hospital cardiac arrest due to ventricular fibrillation after ECG signs of coronary spasm. Coronary artery disease was excluded. Ergonovine provocation induced coronary spasm in this patient. This is, to the authors' knowledge, the first description of ventricular fibrillation in EIA, possibly due to coronary spasm.

Alpha-adrenoceptors, adrenaline, and exaggerated vasoconstrictor response to stress in essential hypertension.

Stressful sympathetic stimulation by cold pressor test in patients with essential hypertension results in an exaggerated response of the already elevated plasma adrenaline, heart rate, blood pressure, and alpha-adrenoceptor-mediated vasoconstriction when compared with normotensive subjects. The stress-induced increase in adrenaline was correlated with the attendant increase in blood pressure. The stress-induced reduction in forearm flow was reversed during infusion of the postjunctional alpha 1-adrenoceptor blocker prazosin. Therefore, enhanced responses to sympathetic stress, as reflected and perhaps caused by an exaggerated rise in plasma adrenaline, may contribute to an increased alpha 1-adrenoceptor-mediated vasoconstriction in essential hypertension.

Coronary pseudoaneurysm: diagnosis by intravascular ultrasonography.

A pseudoaneurysm after percutaneous coronary angioplasty (PTCA) of the left anterior descending coronary artery is reported in a 52-year-old woman who underwent PTCA for exertional angina and a significant isolated stenosis of the left anterior descending coronary artery. Intravascular ultrasonography during repeat coronary angiography clearly identified a localized coronary dilation at the PTCA site in conventional coronary angiography as a pseudoaneurysm that was confirmed during surgery.

A reversible form of apical left ventricular hypertrophy associated with pheochromocytoma.

A patient with pheochromocytoma was found to have typical features of apical left ventricular hypertrophy similar to apical hypertrophic cardiomyopathy of the Japanese type. The electrocardiogram showed giant negative T waves (1.0 mV), and echocardiography as well as angiographic examination revealed left ventricular hypertrophy confined to the apex. Surgical removal of the tumor resulted in striking regression of apical hypertrophy and essential normalization of the electrocardiogram within 1 year of operation. These findings emphasize the possible role of catecholamines in the cause of apical hypertrophic cardiomyopathy and illustrate the potential reversibility of this condition in association with pheochromocytoma. It is suggested that patients with signs of apical left ventricular hypertrophy should undergo thorough screening for a pheochromocytoma.

Treatment of internal mammary artery malperfusion syndrome by additional venous graft: early postoperative angiographic results.

BACKGROUND: Internal mammary artery malperfusion syndrome is caused by an acute imbalance between myocardial demand and nutritional support through the mammary artery. METHODS: We performed early angiography in 11 consecutive patients in whom the perioperative course suggested mammary artery malperfusion. All patients received an additional saphenous vein graft distally to the mammary artery anastomosis. RESULTS: Postoperative angiography revealed patent mammary artery and vein graft in 10 patients (three with a markedly reduced caliber of the arterial graft). CONCLUSION: Additional vein graft is the treatment of choice in mammary artery malperfusion syndrome; it does not lead to occlusion of the internal mammary artery.

Surgical revascularization in acute myocardial infarction.

To determine the potential benefit of myocardial revascularizations in acute myocardial infarction we analyzed a consecutive series of 641/3397 patients with stable or unstable angina in Canadian Heart Association Class IV divided into five groups: A) unstable angina (ECG S-T modifications), B) evolving infarction (new Q-wave, CK more than 3 times normal), C) mechanical complications (ventricular septal defect (VSD), wall rupture, acute mitral regurgitation), D) coronary artery occlusion (crashed percutaneous transluminal coronary angioplasty (PTCA)), and E) stable angina class IV (control group). The mean follow-up was 72 +/- 33 months (range 24-144 months). Of the 641 patients 362 were unstable (A), 22 had evolving infarction (B), 20 suffered from mechanical complications (C), 48 had acute coronary artery occlusion (D), and 189 were in the control group (E). There was no difference for left ventricular (LV) ejection fraction before surgery (P < 0.05 = * as compared to control (E)), however cardiogenic shock was present before surgery in 13/362 (4%) for unstable angina, 5/22 (23%) for evolving infarction, 6/20 (30%) for mechanical complications, 4/48 (8%) for acute occlusion, and none of the controls. The number of bypasses was 3.8 +/- 1.3* for unstable angina, 3.6 +/- 1.3 for evolving infarction, 2.3 +/- 1.2* for mechanical complications, 2.0 +/- 1.2* for acute occlusion, and 3.4 +/- 1.5 for control. Intra-aortic balloon pumping was necessary in 26/362 (7%) for unstable angina, 5/22 (23%*) for evolving infarction, 7/20 (35%*) for mechanical complications, 7/48 (15%*) for acute occlusions, and 5/189 (3%) of the controls.(ABSTRACT TRUNCATED AT 250 WORDS)

The internal mammary artery malperfusion syndrome: incidence, treatment and angiographic verification.

Internal mammary artery (IMA) malperfusion syndrome is caused by an acute imbalance between myocardial demand and nutritional support through the mammary artery. In a consecutive series of 2326 isolated myocardial revascularizations-with at least one IMA to the left anterior descending branch (LAD) in 91.3% (2125/2326)-we identified 45 patients (1.9%) with a perioperative course suggesting IMA malperfusion syndrome. Additional saphenous vein graft to the distal segment of the LAD was performed during normothermic ventricular fibrillation in all patients. Hospital mortality was 4.4% (2/45), intra-aortic balloon pumping was required in 15.5% (7/45) and anterior myocardial infarction occurred in 28.8% (13/45). Coronary angiography was performed in all survivors between 3 and 24 months postoperatively. Wide patent IMA graft and patent saphenous vein graft were observed in 56% (24/43), narrowed but patent IMA graft and patent vein graft in 35% (15/43), while patent vein graft and not visualized IMA in 7% (3/43); in one patient with severely diseased peripheral LAD, no flow could be demonstrated in the IMA graft or in the additional vein graft (1/43, 2.4%). No major differences were found between early and late coronary angiography in these patients. Additional vein graft to distal LAD is the treatment of choice in acute IMA malperfusion syndrome. Despite patent vein graft with superior blood flow, early and late postoperative IMA flow to LAD is maintained in the majority of patients.

Post-prandial lipaemia and endothelial function among healthy men.

BACKGROUND: There is evidence that elevated post-prandial lipoproteins adversely affect progression and outcome of cardiovascular disease. Traditional risk factors are associated with impaired endothelium-mediated vasodilatation. However, studies regarding the relationship between post-prandial lipaemia and endothelial function are divergent. METHODS: Twelve healthy non-smokers were included in this study. Before and after intake of a lipid cocktail rich in dairy fat, we tested endothelial-dependent (acetylcholine 0.8-160 mg/min per 100 ml forearm tissue) and -independent (sodium nitroprussid 0.6 microgram/min) vascular function in the forearm vascular bed with plethysmography. Moreover, we tested the effect of 1-NMMA, a competitive inhibitor of the NO synthetase, on base-line flow. Extent of post-prandial lipaemia was assessed with the increases in triglycerides and retinyl-palmitate, a marker for intestinally derived lipoproteins. RESULTS: Baseline flow was higher after the test meal than during fasting (preprandial 6.5 +/- 0.5 ml/min* 100 ml tissue, post-prandial 8.0 +/- 0.5, p = 0.03), but similar after 1-NMMA (p = 0.85). Before and after intake of the test meal, there was no significant difference in acetylcholine-induced endothelium-dependent vasodilatation (repeated measurement ANOVA, p = 0.22). At the highest acetylcholine dose, forearm flow was very similar (fasting 18.4 +/- 1.9, post-prandial 17.9 +/- 1.9, p = 0.75). At maximum acetylcholine dose, there was a weak inverse but non-significant correlation between forearm flow and post-prandial triglyceridaemia (r = -0.38, p = 0.23) and intestinally derived lipoproteins (chylomicrons r = -0.29, p = 0.35, chylomicron remnants r = -0.15, p = 0.63). However, at the lowest acetylcholine dose there was a suggestion for a positive correlation between change in flow and post-prandial lipaemia (triglyceridaemia, r = 0.53, p = 0.07; chylomicrons, r = 0.41, p = 0.18 and remnants, r = 0.51, p = 0.09). Endothelium-independent vasodilatation in response to sodium nitroprusside did not significantly change (p = 0.23). CONCLUSION: Our results suggest that among healthy men post-prandial lipaemia is not associated with a notable impairment of endothelium-mediated vascular function in forearm resistance vessels.

Sudden cardiac death after aortic valve surgery: incidence and concomitant factors.

A retrospective analysis of 599 consecutive patients after aortic valve surgery aged 7-82 years (mean 56) was performed. During a follow-up of 1-14 years (mean 4.7 years) a 4-week perioperative mortality of 6.9% and a late annual mortality of 3.6% were observed. Sudden cardiac death was the most frequent single cause of death, accounting for 24% of all deaths. Patients dying suddenly were younger than patients dying from other causes (51 +/- 17 vs. 59 +/- 14 years, p less than 0.05) and showed more left ventricular hypertrophy by electrocardiographic criteria when compared with matched survivors (mean Estes score 5.2 +/- 2.4 vs. 2.8 +/- 1.9; p less than 0.01) and with patients dying nonsuddenly (mean Estes score 5.2 +/- 2.4 vs. 1.8 +/- 1.8; p less than 0.01). Ventricular premature beats in the resting electrocardiogram were more prevalent in patients dying suddenly than in matched survivors (55 vs. 20%; p less than 0.025) as well as in patients dying from other causes (55 vs. 25%; p less than 0.05). In addition, there were more intracardiac conduction disturbances and more ungrafted coronary vessels with insignificant stenoses at the time of surgery in sudden death patients. Our findings suggest that after aortic valve replacement patients with left ventricular hypertrophy, bundle-branch block, and ventricular premature beats in the resting electrocardiogram are at increased risk for sudden cardiac death. A possible etiological role of concomitant coronary artery disease must be considered.

Reversal of atherosclerotic obstructions by percutaneous transluminal angioplasty raises high-density lipoprotein cholesterol.

Variation of high-density lipoprotein cholesterol (HDL) levels in man show a strong inverse relationship to the incidence of atherosclerotic vascular disease. Conversely, effects of atherosclerosis and ischemia on lipoprotein metabolism are unclear. We investigated 41 patients, 10 women and 31 men, undergoing percutaneous transluminal angioplasty by measuring fasting lipoprotein cholesterol including high-density lipoprotein subfraction analysis before and one as well as 12 weeks after the procedure. Successful reopening of a haemodynamically significant iliac, femoral or popliteal obstruction was achieved in all patients. A highly significant (p < 0.001) increase of HDL cholesterol from 1.10 +/- 0.05 to 1.31 +/- 0.06 mmol/l was revealed 12 weeks later. This was due to a significant (p < 0.001) increase in HDL3 cholesterol by 26%, whereas HDL2 cholesterol did not change significantly. We conclude that HDL cholesterol levels increase after recanalization of a significant atherosclerotic obstruction which may be a direct effect of reperfusion or an indirect effect due to an increase in exercise tolerance.

[Coronary stents]. / Koronare Stents.

Since the introduction of coronary stents into clinical practice in the late 1980s, the number of stent implantations has increased so rapidly that stents are currently used in over 80 percent of all percutaneous coronary interventions. Although stent implantation was initially limited to large vessels with proximal and discrete lesions, improvements in stent design and implantation technique now allow their deployment in more complex lesions in smaller and diffusely diseased vessels. The overall acceptance of stents by interventional cardiologists can be attributed to favorable acute and longterm results compared to balloon angioplasty alone. Interventionalists have also been quick to embrace the smoother and larger lumen after stenting, in a shorter procedure time and with no additional risk, especially since the risk of stent thrombosis has been overcome by the introduction of dual antiplatelet therapy with Aspirin and Ticlopidine or Clopidogrel. Although restenosis and the need for reinterventions is lower after stenting compared to balloon angioplasty it still remains significant with about 15 percent of all patients returning for an other revascularization procedure. Meanwhile, a completely new generation of stents promises to eliminate the problem of restenosis. Drug-eluting stents, coated with antiproliferative substances have been successfully tested in small randomized trials. The restenosis rates at 6 and 12 months were extremely low ranging between zero and nine percent, with no clinical drawbacks so far. If these results hold up in longer follow up and in real life practice with more complex lesions stented the treatment of symptomatic coronary artery disease will change even more dramatically.