An approach to shorten time to infarct artery patency in patients with ST-segment elevation myocardial infarction.

We developed a regional strategy to decrease the time to percutaneous coronary intervention (PCI) for patients with acute ST-segment elevation myocardial infarction (STEMI). Protocols were created for paramedics and referring hospitals to identify and directly triage all patients with STEMI to a single PCI center. Time to PCI reperfusion and in-hospital mortality were assessed in 233 consecutive patients with STEMI. Ninety-minute initial hospital door-to-patent infarct artery was achieved in 58.3% of paramedic-diagnosed and directly triaged patients compared with 37.5% of "walk-ins" to the PCI hospital and with only 5.2% of those transferred from another hospital emergency department (ED; p <0.001). Overall in-hospital mortality was 2.1%, 0% in paramedic identified patients, and 0% in those walk-ins to the PCI hospital ED compared with 4.3% for those transferred from a referring hospital ED (p = 0.007). Paramedic diagnosis of STEMI and direct triage to a prealerted interventional hospital for primary PCI was associated with a high percentage of patients achieving <90-minute infarct artery patency. Substantial delays remained for those who presented initially to a non-PCI hospital ED despite the expedited protocol. In conclusion, this observational study suggests that wider use of paramedic electrocardiographic STEMI diagnosis and direct triage to a prealerted PCI hospital catheterization team may help improve outcomes of patients with STEMI.

Left main dissection and thrombosis in a young athlete.

Spontaneous coronary artery dissection is a rare but morbid event. We present the case of a previously healthy 38-year-old man who experienced severe chest discomfort while vigorously exercising. An acute anterolateral myocardial infarction was diagnosed. The patient underwent coronary angiography, demonstrating acute thrombosis of the left main coronary artery. The patient was referred for immediate bypass surgery. Examination of the left main coronary artery in the operating room revealed a dissection flap with thrombosis. With successful surgical intervention, the patient made an uneventful recovery. This case is discussed and the literature reviewed.

Correlates of coronary blood flow before and after percutaneous coronary intervention and their relationship to angiographic and clinical outcomes in the RESTORE trial. Randomized Efficacy Study of Tirofiban for Outcomes and REstenosis.

BACKGROUND AND OBJECTIVES: Slower blood flow in the setting of acute myocardial infarction (MI) has been related to adverse outcomes, but the relationship of coronary blood flow after percutaneous transluminal coronary angioplasty (PTCA) in the setting of acute coronary syndromes to adverse outcomes and restenosis has not been well described. We sought to evaluate the correlates of pre- and post-PTCA coronary blood flow to shed light on potential modifiable determinants. METHODS: The RESTORE trial (Randomized Efficacy Study of Tirofiban for Outcomes and REstenosis) was a randomized, double-blind, placebo-controlled trial of tirofiban in patients undergoing balloon angioplasty or directional atherectomy within 72 hours of occurrence of either unstable angina pectoris or acute MI. Coronary blood flow was assessed with the corrected TIMI frame count (CTFC), and clinical outcomes were assessed at 30 days. RESULTS: In addition to tighter and longer minimum lumen diameters (MLDs), the multivariate correlates of slower flow before PTCA also included the presence of thrombus, collaterals, left coronary artery lesion location, acute MI, and >8F catheter size. As well as the above variables, type C and D dissection grades were related to slower post-PTCA CTFC. Death, or the composite of death/MI/coronary artery bypass graft at 30 days, was more frequent among patients with slower post-PTCA CTFCs and those with post-PTCA thrombus. In a multivariate model correcting for reference segment diameter and MLD, the post-PTCA CTFC was an independent predictor of late lumen loss and the follow-up MLD at 6 months. As a single index that integrates functional and anatomical aspects of the post-PTCA results, the ratio of CTFC/MLD was associated with death/MI by 30 days. CONCLUSIONS: In addition to MLD, variables such as the presence of thrombus, left coronary artery lesion location, and dissection grade also are associated with slower coronary blood flow after PTCA. In turn, post-PTCA CTFCs were an independent predictor of late lumen loss and follow-up MLDs. Furthermore, patients who die or who sustain other adverse cardiac events have slower coronary blood flow and greater thrombus burden after PTCA.

Angiographic and clinical characteristics associated with the development of Q-wave and non-Q-wave myocardial infarction in the thrombolysis in myocardial infarction (TIMI) 14 trial.

BACKGROUND: In the absence of thrombolytic therapy, patients with non-Q-wave myocardial infarction (MI) have previously been shown to have lower long-term mortality rates than patients with Q-wave MI. The goal of our study was to examine the angiographic and clinical differences between non-Q-wave MI and Q-wave MI in patients with ST elevation MI (STEMI) in the era of thrombolytic and combination therapy of thrombolytics plus glycoprotein IIb/IIIa inhibitors. METHODS: Angiography was performed 90 minutes after thrombolytic administration in the Thrombolysis in Myocardial Infarction (TIMI) 14 trial. The development of a non-Q-wave MI was assessed on electrocardiogram performed at the time of hospital discharge. Angiographic findings were assessed at an angiographic core laboratory by blinded investigators. RESULTS: The qualifying episode of ST elevation developed into a non-Q-wave MI in 36% of patients (315/878) and into a Q-wave MI in 64% of patients (563/878). In patients in whom non-Q-wave MI developed, the rate of TIMI grade 3 flow was higher, peak creatine kinase level was lower, mean left ventricular ejection fraction was greater, corrected TIMI frame counts (CTFCs) were lower (ie, faster blood flow), and chest pain duration after thrombolytic administration was shorter. Patients in whom non-Q-wave MI developed less frequently underwent a percutaneous coronary intervention (PCI), and when they did, they had faster post-PCI CTFCs and higher rates of post-PCI TIMI grade 3 flow. Patients in whom a non-Q-wave MI developed had lower rates of severe recurrent ischemia. There were no differences in 30-day or in-hospital mortality rates or recurrent MI between patients with Q-wave MI and patients with non-Q-wave MI. CONCLUSION: After thrombolytic therapy in STEMI with or without abciximab, ejection fractions were higher, the duration of ischemia was shorter, and coronary blood flow at both 90 minutes and after PCI was faster in patients who sustained non-Q-wave MI than in patients who sustained Q-wave MI. No differences in mortality or recurrent MI rates were detected in patients who sustained a Q-wave MI and patients in whom a Q-wave MI did not evolve in the modern thrombolytic era.

Intracardiac echocardiography during transcatheter interventions for congenital heart disease.

Although transesophageal echocardiography is often used for guidance during transcatheter interventions, few data exist regarding the use of the newer modality of intracardiac echocardiography. This brief report summarizes our single center experience using intracardiac echocardiographic guidance during transcatheter interventional procedures for congenital heart disease.

Pretreatment with intragraft verapamil prior to percutaneous coronary intervention of saphenous vein graft lesions: results of the randomized, controlled vasodilator prevention on no-reflow (VAPOR) trial.

BACKGROUND: Intragraft verapamil is effective in treating no-reflow during saphenous vein graft (SVG) percutaneous coronary intervention (PCI). In this study, we assessed the use of intragraft verapamil given pre-PCI to prevent no-reflow. METHODS: Patients undergoing SVG PCI were randomized to receive intragraft 200 g verapamil or no verapamil immediately prior to PCI. Pre- and post-PCI, vessel flow was assessed using TIMI flow grade and TIMI frame count by blinded angiographic readers. Tissue level perfusion in the graft territory was assessed using the TIMI myocardial perfusion grade (TMPG). CK-MB or troponin I levels were measured 6 12 hours post-PCI. RESULTS: Ten patients were randomized to the verapamil group and 12 were assigned to the placebo group. No-reflow occurred in 33.3% of the placebo group, compared to none of the verapamil patients (p = 0.10). The use of intragraft verapamil prior to SVG PCI increased flow rate in the vessel as assessed by TIMI frame count (53.3 22.4% faster in the verapamil group versus 11.5 38.9% in the placebo group; p = 0.016). There was a trend toward improved myocardial perfusion as assessed by TMPG. There was no difference in the incidence of cardiac biomarker release following PCI. CONCLUSIONS: Intragraft administration of verapamil prior to saphenous vein graft PCI reduces no-reflow and is associated with a trend toward improved myocardial perfusion.

Is there any indication for aortic valvuloplasty in the elderly?

Elderly patients with severe symptomatic calcific aortic stenosis do poorly with medical management. The optimal treatment for this group of patients is surgical valve replacement. Balloon valvuloplasty may be useful as a bridge to aortic valve replacement in hemodynamically unstable patients, in patients undergoing emergent noncardiac surgery, and in patients with severe comorbidities who are too ill to undergo cardiac surgery. Balloon valvuloplasty often results in symptomatic improvement; however, the postvalvuloplasty valve area is usually <1.0 cm2, the major periprocedural complication rate is roughly 5%, and the 6-month restenosis rate is quite high. There is no evidence that balloon valvuloplasty alters the natural history of aortic stenosis, although no randomized study has been performed.

Optimal treatment and current situation in reperfusion after thrombolysis for acute myocardial infarction.

Acute myocardial infarction is the leading cause of death in the industrialized world and the paramount goal is establishing early, complete, and sustained reperfusion at the myocardial tissue level. For hospitals without the capacity to perform emergent percutaneous coronary intervention, fibrinolytic therapy plays a critical role although it is limited by a 67% success rate. Despite promising pilot studies, reduced-dose fibrinolytic therapy with glycoprotein IIb/IIIa therapy (GUSTO-V) and full-dose fibrinolytic therapy with enoxaparin (ASSENT-3) or bivalirudin (HERO-2) provide only marginally improved clinical outcomes. Adjunctive in-hospital and secondary preventive measures should include an aspirin, a beta-blocker, an ACE inhibitor, and a statin, based on the Heart Protection Study, unless contraindicated. Patients should be risk stratified, participate in a cardiac rehabilitation program, cease smoking tobacco, and have an intracardiac defibrillator (ICD) implanted if their LV systolic function is < or = 30% at one month based on the MADIT-2 trial.

Methodologic and clinical validation of the TIMI myocardial perfusion grade in acute myocardial infarction.

Improved microvascular perfusion using the TIMI myocardial perfusion grade (TMPG) has been related to reduced in hospital, 30-day and 2-year mortality following thrombolytic administration. We sought to validate this measure using the more quantitative technique of digital subtraction angiography (DSA) and to correlate TMPG with ST segment resolution. DSA was used to analyze films from the LIMIT AMI acute myocardial infarction trial of front loaded r-tPA and rhuMAb CD18. Dye kinetics were also characterized using DSA in 88 arteries from patients without acute coronary syndromes in the absence of an obstructive lesion. Compared to normal patients, microvascular perfusion was reduced in acute myocardial infarction patients on DSA as demonstrated by a reduction in peak Gray (brightness) (p < 0.0001), the rate of rise in Gray/sec (p < 0.0001), the blush circumference (p < 0.0001), and the rate of growth in circumference (cm/sec) (p < 0.0001). However, while DSA perfusion was impaired overall in the setting of acute myocardial infarction, TMPG grade 3 in the setting of acute myocardial infarction did not differ from that in normal patients when studied quantitatively as shown by similar rates of growth in brightness and circumference (p = NS). ST resolution and the TMPG were significantly associated (p = 0.04). Compared to normal patients, acute myocardial infarction reduces the peak brightness of the myocardium, the rate of rise in brightness, the circumference of blush and the rate of growth in circumference as assessed using digital subtraction angiography. However, acute myocardial infarction patients with TMPG 3 had rates of growth in brightness and circumference that were nearly identical to normal patients. Thus, DSA validates that TMPG 3 is associated with normal kinetics of myocardial perfusion, and this likely accounts for the low (0.7%) 30 day mortality observed among those patients with TFG 3 and TMPG 3.