Several multicenter studies have suggested that in the above patients, an initial management strategy of PCI+MT does not reduce the long-term risk of cardiovascular events more effectively than initial MT only.

We conducted a randomized comparative study (JSAP [Japanese Stable Angina Pectoris] study) in the previously mentioned patients.

The patients were randomized to PCI+MT (n = 192) or initial MT only group (n = 192), and the patient characteristics were very similar in the 2 groups. During the 3.3-year follow-up, there was no significant difference in the cumulative death rate between PCI+MT (2.9%) and MT (3.9%). However, the cumulative risk of death plus acute coronary syndrome was significantly smaller in PCI+MT.

In stable low-risk CAD, PCI+MT may improve long-term prognosis more effectively than MT.

It is uncertain whether percutaneous coronary interventions (PCI) or coronary artery bypass grafting (CABG) surgery provides better clinical outcomes among patients with single-vessel disease of the proximal LAD.

We searched relevant databases (MEDLINE, EMBASE, and Cochrane from 1966 to 2006) to identify randomized controlled trials that compared outcomes for patients with single-vessel proximal LAD assigned to either PCI or CABG.

We identified 9 randomized controlled trials that enrolled a total of 1,210 patients (633 received PCI and 577 received CABG). There were no differences in survival at 30 days, 1 year, or 5 years, nor were there differences in the rates of procedural strokes or myocardial infarctions, whereas the rate of repeat revascularization was significantly less after CABG than after PCI (at 1 year: 7.3% vs. 19.5%; at 5 years: 7.3% vs. 33.5%). Angina relief was significantly greater after CABG than after PCI (at 1 year: 95.5% vs. 84.6%; at 5 years: 84.2% vs. 75.6%). Patients undergoing CABG spent 3.2 more days in the hospital than those receiving PCI (95% confidence interval: 2.3 to 4.1 days, p < 0.0001), required more transfusions, and were more likely to have arrhythmias immediately post-procedure.

In patients with single-vessel, proximal LAD disease, survival was similar in CABG-assigned and PCI-assigned patients; CABG was significantly more effective in relieving angina and led to fewer repeat revascularizations.

Data are limited regarding uniform evaluation of ST and the influence of clopidogrel continuation beyond 12 months on late events after DES treatment.

We identified 7,221 patients who received DES implantation (n = 3,160) or bare-metal stent (BMS) implantation (n = 4,061), and compared long-term adverse outcomes. Additionally, 2,851 patients with DES surviving 12 months without major events were analyzed according to clopidogrel continuation.

The adjusted-risk of overall ST was similar in the 2 groups. After 1 year, however, DES patients showed a higher risk of ST; definite/probable (hazard ratio [HR]: 3.55, 95% confidence interval [CI]: 1.26 to 9.99). The adjusted-risk of death (HR: 0.60, 95% CI: 0.46 to 0.79), death/myocardial infarction (HR: 0.63, 95% CI: 0.49 to 0.81), and target lesion revascularization (HR: 0.32, 95% CI: 0.24 to 0.43) were significantly lower in the DES group than in the BMS group. Continuing clopidogrel beyond 12 months was not associated with a reduced risk for ST (HR: 0.54, 95% CI: 0.07 to 4.23), death (HR: 1.20, 95% CI: 0.55 to 2.66), or death/myocardial infarction (HR: 1.16, 95% CI: 0.56 to 2.42) after DES implantation.

As compared with BMS, DES showed a similar risk of overall ST, but a higher risk of very late ST. The rates of death, death/myocardial infarction, and target lesion revasuclarization were significantly lower in the DES group. Clopidogrel continuation beyond 1 year did not appear to reduce ST and clinical events after DES implantation.

Time to reperfusion is a major determinant of mortality among STEMI patients. Rapid initiation of fibrinolytic therapy can shorten time to reperfusion, and mechanical therapy of the culprit lesion is known to be beneficial.

Data from 2,869 STEMI patients treated in 5 high-volume percutaneous coronary intervention (PCI) centers were pooled for analysis. Mortality at 30 days was the primary end point. Death, reinfarction, and stroke were secondary end points, as were infarct-related artery TIMI (Thrombolysis In Myocardial Infarction) flow grade before PCI and shock on arrival to the catheterization laboratory.

Compared to PPCI, mortality at 30 days was significantly lower with FAST-PCI (3.8% vs. 6.4%, p = 0.002). The combined triple end point of death, reinfarction, or stroke was also less frequent (5.1% vs. 8.9%, p < 0.0001). The FAST-PCI patients had a lower incidence of Killip class IV (5.6% vs. 10.9%, p < 0.0001) and higher infarct-related artery TIMI flow grades (2.1 ± 1.2 vs. 1.1 ± 1.3, p < 0.0001) upon arrival in the catheterization laboratory. Stepwise logistic regression analysis demonstrated that FAST-PCI was an independent predictor of 30-day mortality (relative risk = 0.542, p = 0.0151).

The FAST-PCI strategy reduced the mortality and combined end point of death, reinfarction, and stroke among STEMI patients, without increasing the risk of stroke or bleeding, compared to PPCI. Fibrinolysis before hospital admission also increased the initial infarct-related artery patency and decreased the likelihood of shock at presentation.

Previous studies in patients with acute coronary syndromes suggest that the impact of infarct-related artery recanalization on clinical outcome is greatest in patients at highest risk.

Of 2,201 patients (age 58.6 ± 11.0 years) with infarct-related artery occlusion on days 3 to 28 after myocardial infarction in the OAT (Occluded Artery Trial) study, 1,101 were assigned to percutaneous coronary intervention (PCI) and 1,100 to medical therapy alone and followed for a mean of 3.2 years. The primary end point was a composite of death, reinfarction, or New York Heart Association functional class IV heart failure. Interaction of treatment effect with tertiles of predicted survival were examined using the Cox survival model.

The 5-year rate for the primary end point was 18.9% versus 16.1% for patients assigned to PCI and medical treatment alone, respectively (hazard ratio [HR]: 1.14, 95% confidence interval [CI]: 0.92 to 1.43, p = 0.23). Lack of benefit of PCI was consistent across the risk spectrum for both the primary end point and total mortality, including for the highest tertile (33.9% PCI vs. 27.3% medical treatment alone, HR: 1.27, 99% CI: 0.87 to 1.85 primary end point and 23.5% PCI vs. 21.7% medical treatment alone, HR: 1.16, 99% CI: 0.73 to 1.85 mortality). The independent predictors of the composite outcome were history of heart failure (HR: 2.06, p < 0.001), peripheral vascular disease (HR: 1.93, p = 0.001), diabetes (HR: 1.49, p = 0.002), rales (HR: 1.88, p < 0.001), decreasing ejection fraction (HR: 1.48 per 10%, p < 0.001), decreasing days from myocardial infarction to randomization (HR: 1.04 per day, p < 0.001), and decreasing glomerular filtration rate (HR: 1.11 per 10 ml/min/1.73 m², p < 0.001).

In the OAT study, there was no variation in the effect of PCI on clinical outcomes at different levels of patient risk, including the subset with very high event rates. (Occluded Artery Trial [OAT]; NCT00004562)

The ZoMaxx stent system elutes 10 µg/mm zotarolimus using a phosphorylcholine polymer loaded onto a novel stainless steel stent platform containing a 0.0007-inch inner layer of tantalum.

Twenty-nine investigative sites in Europe, Australia, and New Zealand enrolled 401 patients, 396 of whom received a study stent.

After 9 months, late lumen loss was significantly greater in the ZoMaxx group (in-stent 0.67 ± 0.57 mm vs. 0.45 ± 0.48 mm; p < 0.001; in-segment 0.43 ± 0.60 mm vs. 0.25 ± 0. 45 mm; p = 0.003), resulting in significantly higher rates of >50% angiographic restenosis (in-stent 12.9% vs. 5.7%; p = 0.03; in-segment 16.5% vs. 6.9%; p = 0.007). The upper bound of the 95% confidence interval on the difference in in-segment late lumen loss between the 2 treatment groups (0.27 mm) exceeded the 0.25 mm value pre-specified for noninferiority. There were no significant differences between ZoMaxx and Taxus-treated groups with respect to target lesion revascularization (8.0% vs. 4.1%; p = 0.14), major adverse cardiac events (12.6% vs. 9.6%; p = 0.43), or stent thrombosis (0.5% in both groups).

After 9 months, the ZoMaxx stent showed less neointimal inhibition than the Taxus stent, as shown by higher in-stent late loss and restenosis by qualitative coronary angiography.

Inflammatory responses to polymers and delayed healing remain important safety issues associated with CDES. Whether nonpolymeric stents that elute sirolimus or sirolimus and estradiol provoke less inflammation and heal better is unknown.

Twenty-eight rabbits received 2 overlapping stents in each iliac artery: SES, SES+ED, BMS, or CDES, and vessels were harvested at 28 days for histology and scanning electron microscopy.

Although similar at nonoverlapping segments, neointimal thickness within the overlap site of CDES was significantly less than in SES, SES+ED, and BMS (0.07 ± 0.04 mm vs. 0.16 ± 0.03 mm, 0.14 ± 0.03 mm, and 0.15 ± 0.03 mm, p < 0.0001). Endothelialization was greater in SES, SES+ED, and BMS compared with CDES in nonoverlapping sections (80.0 ± 5.0% vs. 95.3 ± 5.0%, 97.5 ± 2.5%, and 96.7 ± 3.8%; p = 0.0028) and overlapping sections (85.8 ± 2.9% vs. 90.8 ± 6.3%, 89.2 ± 6.3%, and 48.3 ± 2.9%; p < 0.0001). The number of luminal eosinophils was also less in overlapping sections of SES, SES+ED, and BMS versus CDES but was similar in nonoverlapping sections.

Polymer-free stents coated with SES or SES+ED result in less robust neointimal suppression but markedly improved arterial healing compared with CDES in the rabbit model.

Recent concerns regarding the long-term safety of drug-eluting stents have been raised. Synthetic polymers have been associated with intensive inflammatory response and late stent thrombosis. Newly developed, the VES combines a stainless steel platform with a nanothin-microporous hydroxyapatite surface coating impregnated with a polymer-free sirolimus formulation (55 µm).

In May 2007, 15 patients with single de novo lesion located in native coronary arteries 3.0 to 3.5 mm in diameter and ≤14 mm in length were consecutively enrolled. Primary end points included in-stent late lumen loss and in-stent percent of obstruction at 4 months. Serial angiography and intravascular ultrasound were obtained at the index procedure and repeated at 4-month follow-up.

Mean population age was 63.8 years; 33% of patients were diabetic. The left anterior descending artery was the prevalent target vessel (47%). Reference vessel diameter and lesion length were 2.67 ± 0.32 mm and 9.98 ± 1.98 mm, respectively. The VES was successfully implanted in all cases, and there were no procedure and in-hospital complications. Life-long aspirin and 6-month clopidogrel therapy were prescribed for all patients. At 4 months, in-stent late lumen loss was 0.30 ± 0.25 mm and percent of stent obstruction was 2.8 ± 2.2%. After up to 6 months of clinical follow-up, no major adverse cardiac event was registered.

The third-generation VES demonstrated excellent acute results in the treatment of de novo coronary lesions. Longer follow-up with a more complex subset of patients and lesions is required to confirm these preliminary results.

Septal ablation is an alternative therapy for patients with obstructive hypertrophic cardiomyopathy (HCM). However, its beneficial effect on diastolic function, by relieving the systolic contraction load, may be countered by adverse effects from the infarction on left ventricular mechanics.

Using high-fidelity, micromanometer-tipped catheters, we examined 40 HCM patients by taking direct measurements of the left ventricular outflow tract (LVOT) gradient, time constant of myocardial relaxation (tau), and left atrial pressure (LAP) before and after septal ablation.

Although there was an overall reduction in LVOT gradient, septal ablation resulted in variable changes in myocardial relaxation and left atrial pressure. In 20 patients (50%), LAP increased. The magnitude of LVOT gradient reduction directly correlated with the effects of septal ablation on LAP (R = 0.58; p < 0.0001). Those patients with a greater decrease in the LVOT gradient had better improvement in direct LAP. Furthermore, those patients with a larger decrease in left ventricular outflow tract gradient had a beneficial enhancement of ventricular relaxation, as measured by tau (R = 0.43; p = 0.006). Thus, the beneficial enhancement of relaxation was directly related to improvement in LAP (R = 0.75; p < 0.0001).

Septal ablation results in variable effects on left ventricular filling pressure, which are dependent upon the magnitude of reduction in the LVOT gradient. These effects are mediated in part by effects of ablation on myocardial relaxation. These findings shed insight into the pathophysiologic effects of septal reduction therapy in patients with HCM.

There are inadequate data on the long-term outcome of ASA for symptomatic hypertrophic obstructive cardiomyopathy (HOCM).

Six hundred and twenty-nine patients were enrolled consecutively (1996 to 2007) and 98.4% (n = 619) underwent ASA with 92% follow-up in 2007. Evaluation included deaths, procedural complications, pacemaker requirement, repeat ASA, and myectomy/valve surgery. Follow-up parameters included angina (Canadian Cardiovascular Society score), dyspnea (New York Heart Association functional class), exercise time, and echocardiographic indices (septal thickness, ejection fraction, resting and provoked gradients).

Ethanol (2.6 ± 1.0 ml) was injected into 1.3 ± 0.5 septal arteries, inducing a septal infarct. Complications included death 1% (n = 6), permanent pacemaker requirement 8.2% (n = 52), coronary dissection 1.3% (n = 8), and worsening mitral regurgitation 0.3% (n = 2). The mean follow-up was 4.6 ± 2.5 years (range: 3 months to 10.2 years). During follow-up, New York Heart Association functional class decreased from 2.8 ± 0.6 to 1.2 ± 0.5 (p < 0.001); Canadian Cardiovascular Society angina score decreased from 2.1 ± 0.9 to 1.0 ± 0 (p < 0.001); and exercise time increased from 4.8 ± 3.3 to 8.2 ± 1.0 (p < 0.001) min. The resting and provoked left ventricular outflow tract gradients decreased progressively (p < 0.001) and remained low during follow-up. The septal thickness decreased from 2.1 ± 0.5 cm to 1.0 ± 0.1 cm (p < 0.001) and the ejection fraction decreased from 68 ± 9% to 62 ± 3% (p < 0.001). The survival estimates at 1, 5, and 8 years were 97%, 92%, and 89%, respectively.

The initial benefits of ASA were maintained during follow-up.

Predominantly clinically silent cerebral ischemia has been observed in up to 50% of patients undergoing emboli-protected CAS. The timing and location of cerebral ischemia has not been sufficiently elucidated.

In 58 patients (69.6 ± 8.3 years) who underwent 59 procedures, diffusion-weighted magnetic resonance imaging (DWMRI) was performed before the intervention and at 2 time points (t ₁ and t ₂) after the intervention.

No patient showed recent cerebral injury before CAS. At t ₁ = 3.5 ± 1.8 h, new ischemic foci, all located in the ipsilateral hemisphere, were observed in 12 of 59 DWMRI studies (20.3%, 95% confidence interval: 11.0% to 32.8%). At t ₂ = 18.0 ± 3.1 h, 7 more DWMRI scans showed recent ischemic foci, and 3 scans in patients with positive scans at t ₁ showed additional foci, for a total of 10 scans (17.0%, 95% confidence interval: 8.4% to 29.0%) documenting late cerebral ischemia. In 4 of these (40%), ischemic foci were located contralaterally. Cerebral ischemia was not associated with overt neurological sequelae out to 30 days in any patient.

The incidence of late cerebral ischemia occurring between 3.5 and 18 h after emboli-protected CAS was 17%. It may occur with equal likelihood in either hemisphere. Preventive measures to possibly reduce the incidence of cerebral embolization should focus not only on the target lesion, but also on the access vasculature. Patients should be monitored and DWMRI delayed for at least 18 h after the intervention.

Despite clinicians' growing experience with THV procedures, the best method of annulus sizing remains unclear.

Twenty-three patients with aortic stenosis (<1.0 cm²) who were undergoing surgical valve replacement were enrolled. Pre-operative echocardiographic measurements of the annulus and computed tomography measurements of valve calcium were made. Intraoperatively, a valvuloplasty balloon of known size and inflatable pressure was inserted into the aortic valve and inflated. The development of intraballoon pressure in addition to the nominal inflation pressure (AIBP) reflected the apposition of balloon and valve. Surgical annulus was measured by cylindrical sizers.

In patients with tricuspid valves, AIBP was generated in 11 of 12 patients when the balloon diameter was greater than the surgically measured annulus, regardless of leaflet calcification (2 of 10 patients when balloon ≤ surgical annulus). In bicuspid valves, high AIBP (~1 atm) was encountered with balloons that were within 1 mm of annulus size, and leaflet dehiscence occurred with larger balloons (n = 2 patients). Annulus size was underestimated by transthoracic echocardiogram and transesophageal echocardiogram compared with surgery (p < 0.001): transthoracic echocardiogram = 21.5 ± 1.8 mm, transesophageal echocardiogram = 22.0 ± 1.6 mm and surgical = 23.2 ± 1.9 mm (range 20 to 27 mm, mode 22 mm).

These data suggest that measuring AIBP during balloon aortic valvuloplasty in tricuspid valves is an important adjunctive measurement of the aortic annulus and may help in determining the appropriate THV size.