Optimization of cardiac resynchronization therapy: echocardiographic vs semiautomatic device algorithms.

Large evidence supports the importance of individualized optimization of cardiac resynchronization therapy in patients with congestive heart failure. The aim of this study was to compare a recently developed intracardiac electrogram (IEGM)-based method with the Doppler echocardiographic (ECHO)-based method to calculate optimal atrioventricular (AV) and interventricular (VV) delays. Ten male patients implanted with a St Jude Medical resynchronization device received AV and VV delay assessment with both the IEGM and the ECHO-based methods. Estimates of the optimal AV and VV delays assessed by the 2 tested methods proved highly comparable. No difference emerged between the IEGM (126.8+/-22.7) and the ECHO (127.3+/-19.8) AV delay values (P=.987). The VV delay suggested by ECHO was highly significantly correlated with the delays calculated by the IEGM method (35+/-27.6 vs 21.31+/-24.31; r(2)=0.78; P<.001). These preliminary data support the evidence that an IEGM based cardiac resynchronization optimization method may be as reliable as a complete ECHO assessment.

Role of TGF-beta1 haplotypes in the occurrence of myocardial infarction in young Italian patients.

BACKGROUND: Transforming growth factor beta 1 (TGF-beta1) gene play an important role in the acute myocardial infarction (AMI), however no investigation has been conducted so far in young AMI patients. In this study, we evaluated the influence of TGF-beta1 polymorphisms/haplotypes on the onset and progression of AMI in young Italian population. METHODS: 201 cases and 201 controls were genotyped for three TGF-beta1 polymorphisms (G-800A, C-509T and Leu10Pro). The main follow-up end-points (mean follow-up, 107 +/- 49 months) were death, myocardial infarction or revascularization procedures. RESULTS: Significant risk factors were smoking (p < 10-4), family history for coronary artery disease (p < 10-4), hypercholesterolemia (p = 0.001) and hypertension (p = 0.002). The C-509T and Leu10Pro polymorphisms showed significant differences (p = 0.026 and p = 0.004) between cases and controls. The most common haplotypes revealed a possible protective effect (GCT, OR 0.75, 95% CI 0.57-0.99, p = 0.042) and an increased risk of AMI (GTC, OR 1.51, 95% CI 1.13-2.02, p = 0.005), respectively. No statistical differences were observed in genotype distribution in the follow-up study between the two groups: 61 patients with subsequent events (13 deaths) and 108 without events. CONCLUSION: Even though our results need to be further confirmed in larger studies, this is the first study reporting on a possible role of TGFbeta1 common haplotypes in the onset of AMI in young patients.

In vivo coronary plaque histology in patients with stable and acute coronary syndromes: relationships with hyperlipidemic status and statin treatment.

OBJECTIVES: Aim of the study was to investigate whether maintained moderate statin treatment influence atheroma, macrophage content, neoangiogenesis and/or haemorrhage in coronary plaques from patients with non-fatal coronary syndromes. METHODS: A total of 48 patients underwent elective directional coronary atherectomy on "de novo" culprit lesions; 16 patients had non-treated hypercholesterolemia, 16 patients received maintained moderate statin treatment for hypercholesterolemia and 16 had no lipoprotein abnormalities. These three patients groups were matched for age and clinical diagnosis of stable angina (SA) or unstable angina/non-ST-elevation myocardial infarction (UA/NSTEMI). Atherectomy specimens were stained with antibodies against macrophages, endothelial cells and glycophorin A. Results of histology and immunohistochemistry were morphometrically analyzed by using computer-assisted image analysis. RESULTS: Atheroma and fibrous tissue, neoangiogenesis, macrophage and haemorrhage (i.e., glycophorin A) differed between the three groups (P<0.05). Statin-treated group showed significantly decreased atheroma (P=0.016), fibrous tissue (P=0.42), macrophage content (P=0.012), neoangiogenesis (P=0.00048) and haemorrhage (P=0.0092) as compared with the non-treated hyperlipidemic group. CONCLUSIONS: The present findings show that maintained moderate statin treatment may contribute to plaque stabilization in non-fatal coronary syndromes by decreasing intraplaque neoangiogenesis and haemorrhage, lipid burden and macrophage content, and, on the other hand, by increasing plaque collagenization.

Sirolimus-Eluting Stents vs Bare Metal Stents for the treatment of unprotected left main coronary artery stenosis.

AIM: This study compares the clinical and angiographic outcomes of sirolimus eluting stent (SES) and bare metal stent (BMS) implantation for unprotected left main coronary artery (ULMCA) stenosis. METHODS AND RESULTS: We analysed 141 unselected patients with unprotected LMCA stenosis: 72 were treated with SES and 69 with BMS. SES patients were younger, with a higher ejection fraction, had more often hypertension, family history and were more often smokers. The procedural success rate was 94.2% in SES group and 87% in BMS group. In SES group there were 2 periprocedural myocardial infarction (3%). 1 intra-procedural death (1.4%) and 1 in-hospital death (1.4%) and respectively 2 (3%),4 (6%) and 3 (4%) in BMS group. No incidents of stent thrombosis, stroke and emergent CABG occurred during hospitalisation in either group. SES patients showed a lower late lumen loss (0.5+/-0.8 mm vs 1.1+/-1.0 mm; p<0.05) and a lower nine-month angiographic restenosis rate (13.6% vs 24.3%; p=NS). The MACE free survival rate at 2 years was 83% in the SES group vs 55% in the BMS group (p<0.001). CONCLUSIONS: SES implantation for unprotected LMCA stenosis in "real world" population appears safe with a low restenosis and MACE rate at follow-up.

Immediate and medium-term outcomes following the treatment of very long (> or =50 mm) chronic total coronary artery occlusions.

OBJECTIVE: The follow-up patency rates and associated clinical and angiographic variables following stenting of very long (> or =50 mm) and chronic (>6 months) total coronary artery occlusive lesions are not well documented. The aim of the present study was to evaluate the early results and mid-term outcomes following angioplasty of such lesions. METHODS: Between January 2000 and June 2002, we treated 278 chronic coronary occlusions. Of these, eighty-nine occlusions (89 patients) were with lesions > or =50 mm long; these patients constituted the study population. RESULTS: Mean duration of occlusion was 7 +/- 2 months (range, 6-13 months). Procedural success was obtained in 81 patients. A total of 211 coronary stents (2.6 +/- 1.1 stents/patient) were implanted, and mean stent length was 59 +/- 9 mm. In 3 patients, TIMI flow 1-2 was observed after stent implantation. Thus, the angiographic success was considered to be 78/89 patients (87.6%). Periprocedural major adverse cardiac events occurred in 6 patients (6.7%). Clinical success was obtained in 74 patients (83%). During a 9.6 +/- 2 month follow-up, forty-three patients (55.1%) remained angina free, thirty-two (41%) had recurrence of angina, three patients (3.9%) had a new myocardial infarction and no deaths were reported. Target vessel revascularization was required in 34 patients (43.6%). Angiographic follow-up was obtained in 70 patients (90%) at a mean of 7.4 +/- 2 months. Restenosis was observed in 36 patients (51%), six of whom had reocclusion. A significant correlation was observed between the need for reintervention and stent length (R 0.52), residual stenosis (R 0.73) and diabetes mellitus (0.68). CONCLUSION: Although coronary artery stenting for very long (> or =50 mm) chronically occlusive lesions is feasible, safe and associated with a low incidence of periprocedural adverse clinical events, these complex and expensive procedures still have a high 6-month restenosis rate. These results might be significantly improved with the advent of drug-eluting stents.

Platelet cyclic GMP levels in unstable angina and myocardial infarction.

BACKGROUND: Several studies showed that there is a state of platelet hyperactivaction in patients with coronary syndrome: the aim of this study is to investigate if the platelet nitric oxide-cyclicGMP (NO-cGMP) pathway, that regulates platelet aggregation is altered in patients with unstable angina (UA) and acute myocardial infarction (AMI). METHODS AND RESULTS: Population included 11 patients with UA, 12 patients with AMI and 23 controls. Platelet cGMP was measured by a radioimmunoassay kit, under basal conditions and after stimulation with sodium nitroprusside (SNP), which maximally stimulates soluble guanylate cyclase (sGC), used as an indirect measurement of active sGC. Basal platelet cGMP values were significantly (P<0.001) higher in patients with UA and AMI than in controls (UA, 1089 +/- 412 pmol/10(10) platelets; AMI, 1071 +/- 507 pmol/10(10) platelets; controls, 492 +/- 201 pmol/10(10) platelets). The final cGMP level reached after SNP stimulation was significantly more elevated in UA, compared with both AMI (P<0.05) and controls (P<0.02) (UA, 4428 +/- 2723 pmol/10(10) platelets; AMI, 2728 +/- 655 pmol/10(10) platelets; controls, 2772 +/- 1031 pmol/10(10) platelets); on the contrary no significant difference between AMI and controls was observed. CONCLUSIONS: Basal platelet cGMP is significantly higher in both UA and AMI groups. This observation suggests that: (1) platelet-derived NO synthesis may be enhanced inUA and AMI, due to increase of intraplatelet calcium level and of platelet cNOS activation; (2) platelets from UA and AMI patients are continuously stimulated by the high-level NO production due to increased iNOS expression. As far as SNP-dependent cGMP production is concerned, UA and AMI behave as two separate conditions. SNP-stimulated activity in UA is higher than in controls, while a loss of functional sGC is observed in AMI.