Keith H. Benzuly

Treatment of no-reflow in degenerated saphenous vein graft interventions: Comparison of intracoronary verapamil and nitroglycerin

No-flow has been reported after 10-15% of percutaneous interventions on degenerated saphenous vein grafts. In this prospective study of 36 degenerated saphenous vein graft lesions (32 patients), no-flow (TIMI flow < 3 in the absence of a significant lesion or dissection) occurred in 15/36 (42%) lesions. A total of 32 episodes of no-flow occurred after angioscopy (n = 14), extraction atherectomy (n = 10), balloon angioplasty (n = 2) or stent implantation (n = 6). Intragraft nitroglycerin (100-300 micrograms) alone resulted in no improvement in TIMI flow in the setting of no-reflow (TIMI flow 1.2 +/- 0.6 to 1.4 +/- 0.8, P = NS). Intragraft verapamil (100-500 micrograms) resulted in improvement in flow in all 32 episodes (TIMI flow 1.4 +/- 0.8 before, to 2.8 +/- 0.5 after verapamil, P < 0.001). Although verapamil increased TIMI flow after all episodes of no-reflow, two (6.3%) had persistent no-reflow (TIMI 1) despite verapamil, associated with non-Q wave myocardial infarction. In conclusion, treatment of no-reflow with verapamil during degenerated vein graft interventions was associated with reestablishment of TIMI 3 flow in 88% of cases. In contrast, intragraft nitroglycerin alone was ineffective for reversing no-reflow.

Functional improvement precedes structural regression of atherosclerosis.

BACKGROUND Vasoconstrictor responses to serotonin are augmented in monkeys with diet-induced atherosclerosis and improve after 18 months of normal diet. We tested the hypothesis that functional improvement may occur early during regression, before evidence of structural improvement. METHODS AND RESULTS Responses of the iliac artery to serotonin were measured by quantitative angiography and a Doppler flow probe in several groups of monkeys: (1) normal monkeys, (2) monkeys fed an atherogenic diet for 2 years (atherosclerotic), and (3) monkeys fed an atherogenic diet for 2 years (preregression) followed by a normal diet for 4, 8, or 12 months (regression). In normal monkeys, serotonin produced minimal constriction of the iliac artery, and blood flow to the legs increased. In atherosclerotic monkeys, there was pronounced constriction of the iliac artery, and blood flow to the legs decreased markedly. After 4 months of regression diet, four of eight monkeys demonstrated marked reduction in hyperresponsiveness to serotonin angiographically, and by 8 months, six of eight monkeys had significant improvement. After regression, serotonin produced minimal changes in flow. There was no reduction in intimal area (ie, atherosclerotic lesion) in iliac arteries from regression monkeys compared with atherosclerotic monkeys, but there was a marked reduction in cholesteryl ester in arteries from regression monkeys. CONCLUSIONS Abnormal vasoconstrictor responses to serotonin usually return to or toward normal within a few months during regression of atherosclerosis. Functional improvement occurs in conjunction with early resorption of lipid from the arterial wall and occurs before detectable changes in mass of the atherosclerotic lesion.

Primary angioplasty reduces risk of myocardial rupture compared to thrombolysis for acute myocardial infarction

Although the mechanical complications of acute ventricular septal defect and acute mitral regurgitation are uncommon after acute myocardial infarction, these complications are associated with an extremely high morbidity and mortality. We hypothesized that the administration of thrombolytic drugs may result in hemorrhagic infarction as well as the potential for incomplete revascularization and thus may lead to an increased incidence of mechanical complications compared to primary angioplasty. Accordingly, we reviewed the data of the most contemporary thrombolytic and primary angioplasty trials and compared the incidence of mechanical complications among 36,303 patients treated with thrombolytics reported in the GUSTO trial to the incidence of mechanical complications among 1,295 patients treated with primary angioplasty obtained from the PAMI-1 and PAMI-2 trials. We found that angioplasty resulted in an overall 86% relative risk reduction in mechanical complications (2.20% vs. 0.31%, P < 0.001). In comparison to thrombolytic therapy, angioplasty resulted in an 82% decrease in acute mitral regurgitation (1.73% vs. 0.31%, P < 0.001) and a 100% decrease in acute ventricular septal defect (0.47% vs. 0.00%, P < 0.03). In conclusion, in patients with acute myocardial infarction, reperfusion with primary angioplasty is associated with less myocardial rupture and mechanical complications than thrombolytics. This finding may, in part, explain the improved prognosis observed in myocardial infarction patients treated with primary angioplasty.

Predictors of long-term outcomes following direct percutaneous coronary intervention for acute myocardial infarction

To determine predictors of a long-term major adverse cardiac event (MACE) in unselected patients undergoing direct percutaneous coronary intervention (PCI), 274 consecutive patients presenting within 12 hours of ST-segment elevation acute myocardial infarction (AMI) were evaluated. No patient with ST-segment elevation AMI received intravenous thrombolytic drugs. Chest pain to balloon time was 3.8 hours (range 2.5 to 6.9). percutaneous transluminal coronary angioplasty was successful in 95% of patients. Abciximab was administered to 69% of patients, stents were deployed in 53%, and 17% underwent only catheterization. In-hospital events were death (7%), abrupt closure (2%), emergent coronary artery bypass grafting (CABG) (5%), repeat PCI (3%), and recurrent myocardial infarction (1%). In patients undergoing direct PCI (n = 227), the in-hospital event rate was death 5.3%, abrupt closure 2.2%, emergency CABG 0.9%, repeat PCI 3.1%, and repeat myocardial infarction 1.3%. Median time to last follow-up or death was 20 months (range 11 to 34), and to any event, 0.3 months (range 0.03 to 24.0). Postdischarge MACE included death (5%), AMI (4%), repeat PCI (8%), CABG (9%), and stroke (0.7%). Among those undergoing direct PCI (n = 227), 10% died, 3.5% had a repeat AMI, 9% had a repeat PCI, 5% had CABG, and 1% had a stroke at long-term follow-up. At long-term follow-up, 75% were event free. Multivariate predictors were (hazard ratio [95% confidence interval (CI)]): abciximab use 0.6 (95% CI 0.43 to 0.95), Killip class 2.2 (95% CI 1.1 to 4.4), and number of narrowed coronary arteries 1.7 (95% CI 1.4 to 2.2). In this unselected consecutive series of patients presenting with ST-segment elevation AMI, direct PCI was associated with sustained long-term efficacy. Outcomes were predicted by cardiac impairment at presentation and number of narrowed coronary arteries. MACE is not related to device selection but is significantly improved with abciximab.

Clinical experience and patient outcomes associated with the TandemHeart percutaneous transseptal assist device among a heterogeneous patient population.

There is a paucity of literature describing the outcomes associated with the use of TandemHeart percutaneous ventricular assist device (PVAD). The literature is limited by analyzing only subsets of patients. We present the clinical outcomes and safety associated with the use of TandemHeart among a series of heterogeneous patients requiring PVAD support. We reviewed the clinical experience, hemodynamic variables, survival outcomes, and complications associated with the implantation of TandemHeart support device among 25 patients presenting to our institution. Indications for PVAD implantation were cardiogenic shock (56%), ST-segment elevation myocardial infarction (STEMI) (20%), postpericardiotomy (16%), and high-risk percutaneous coronary interventions (PCI) or ventricular tachycardia (VT) ablation (8%). TandemHeart was used for an average of 4.8 ± 2.1 days and demonstrated significant hemodynamic improvements (pre- and postimplantation left ventricular ejection fractions were 21.5% ± 15% and 24.5% ± 10.5%, respectively [p = 0.06]). The cardiac index improved from a mean 2.04 ± 075 L/min/m2 to 2.45 ± 073 L/min/m2 (p = 0.09). The mixed venous oxygen saturation (SVO2) increased from 55.14 ± 13.34 to 66.43 ± 7.43 (p = 0.008) after implantation. TandemHeart was used as a bridge to left ventricular assist device implantation (44%) or recovery (20%). Thirty-six percent of patients died on support or shortly after PVAD removal. Thirty, 90-day, and long-term (>90 days) survival rates were 56%, 52%, and 36%, respectively. Procedure-related complications were reported in 13 patients (56%), and the majority (90%) was related to vascular access (bleeding or pseudoaneurysm). The TandemHeart device is a safe therapeutic option as a bridge-to-recovery or bridge-to-bridge for patients with hemodynamic compromise regardless of the etiology. The favorable hemodynamic profile, postimplantation survival rates, and manageable complications support its use to assist hemodynamic recovery in patients refractory to conventional therapy.

Enhanced coronary vasoconstrictive response to serotonin subsides after removal of dietary cholesterol in atherosclerotic monkeys.

Constriction in response to serotonin is enhanced in the coronary arteries of atherosclerotic monkeys. The main objective of the present study was to determine whether abnormal responses to serotonin in atherosclerosis are reversed following removal of dietary cholesterol. In addition, we examined the effect of an atherogenic diet and reduction in dietary cholesterol on vascular responses to activation of ATP-sensitive K+ channels with aprikalim. Diameters of small coronary arteries were measured on the epicardial surface of the left ventricle in vivo by using stroboscopic illumination synchronized to the heart cycle to visually freeze the motion of the heart. Diameters were measured with a microscope-video system during topical application of two vasoconstrictor agonists, serotonin and the thromboxane mimetic U46619, and the vasodilator agonists aprikalim and nitroprusside. Responses were compared in normal (n = 9), atherosclerotic (n = 14; high-cholesterol diet), and regression (n = 8; high-cholesterol diet followed by normal diet) monkeys. Constriction of coronary arteries in response to serotonin was enhanced in monkeys on an atherogenic diet and was normal in regression monkeys. Vasoconstriction in response to U46619 and vasodilation in response to nitroprusside and aprikalim were not altered by atherosclerosis. Thus, abnormal vascular responses to serotonin in small coronary arteries of atherosclerotic monkeys without morphological evidence of disease can be reversed to normal by reducing dietary cholesterol.

Extracellular volume fraction is more closely associated with altered regional left ventricular velocities than left ventricular ejection fraction in nonischemic cardiomyopathy.

Background—Nonischemic cardiomyopathy is a common cause of left ventricular (LV) dysfunction and myocardial fibrosis. The purpose of this study was to noninvasively evaluate changes in segmental LV extracellular volume (ECV) fraction, LV velocities, myocardial scar, and wall motion in nonischemic cardiomyopathy patients. Methods and Results—Cardiac MRI including pre- and postcontrast myocardial T1 mapping and velocity quantification (tissue phase mapping) of the LV (basal, midventricular, and apical short axis) was applied in 31 patients with nonischemic cardiomyopathy (50±18 years). Analysis based on the 16-segment American Heart Association model was used to evaluate the segmental distribution of ECV, peak systolic and diastolic myocardial velocities, scar determined by late gadolinium enhancement, and wall motion abnormalities. LV segments with scar or impaired wall motion were significantly associated with elevated ECV (rs =0.26; P<0.001) and reduced peak systolic radial velocities (r=−0.43; P<0.001). Regional myocardial velocities and ECV were similar for patients with reduced (n=12; ECV=0.28±0.06) and preserved left ventricular ejection fraction (n=19; ECV=0.30±0.09). Patients with preserved left ventricular ejection fraction showed significant relationships between increasing ECV and reduced systolic (r=−0.19; r=−0.30) and diastolic (r=0.34; r=0.26) radial and long-axis peak velocities (P<0.001). Even after excluding myocardial segments with late gadolinium enhancement, significant relationships between ECV and segmental LV velocities were maintained indicating the potential of elevated ECV to identify regional diffuse fibrosis not visible by late gadolinium enhancement, which was associated with impaired regional LV function. Conclusions—Regionally elevated ECV negatively affected myocardial velocities. The association of elevated regional ECV with reduced myocardial velocities independent of left ventricular ejection fraction suggests a structure–function relationship between altered ECV and segmental myocardial function in nonischemic cardiomyopathy.

Late Stent Fractures after Endoluminal Treatment of Ostial Supraaortic Trunk Arterial Occlusive Lesions

PURPOSE Percutaneous catheter-based treatment of supraaortic trunk arterial occlusive lesions obviates the need for extraanatomic bypass or median sternotomy. Although early results have been encouraging, late outcomes have yet to be defined. Reported are long-term outcomes of supraaortic trunk stent placement with particular attention to structural failures. MATERIALS AND METHODS This was a retrospective review of 27 ostial supraaortic trunk lesions managed with balloon-expandable or self-expandable stents. Treated vessels were innominate (n = 9), common carotid (n = 8), and subclavian (n = 10). Access to the target lesion was achieved either antegrade via the femoral artery (n = 13), retrograde through the brachial artery (n = 2), or through a cutdown on the common carotid artery (n = 12). Restenosis and stent integrity were detected with duplex imaging, computed tomography, conventional arteriography, and plain radiography. Mean follow-up time is 34 months. RESULTS Mean age was 68 years (eight men and 19 women), and mean stenosis was 85%. Preprocedural symptoms, including stroke, transient ischemic attack, arm fatigue, digital ischemia, and angina were present in 85% (23 of 27) of the group. At 30 days, there were no deaths, myocardial infarctions, or strokes. During follow-up, three type IV stent fractures in the innominate were detected as well as two midbody stent crush deformities with significant restenosis (one innominate and one common carotid). All stent failures were identified in heavily calcified lesions. CONCLUSIONS Endoluminal stent placement in supraaortic trunk lesions is a viable early solution; however, mid- to long-term restenosis caused by bare metal fatigue and fractures, particularly in cases of calcified innominate artery lesions, are a worrisome finding.

Intraoperative Coronary Artery Dissection in Fibromuscular Dysplasia

A 61-year-old woman with bicuspid aortic stenosis, an ascending aortic aneurysm, and a remote history of renal fibromuscular dysplasia underwent aortic root replacement complicated by extensive dissection of the left circumflex artery extending retrograde into the left anterior descending artery. This was managed by coronary artery bypass grafting, left ventricular support, and percutaneous coronary intervention for propagation of the dissection. This case highlights the prevalence, diagnosis, and management of intraoperative coronary dissection secondary to fibromuscular dysplasia.