Drug-eluting stents versus bare metal stents in ST elevation myocardial infarction: from evidence to practice.

In 2001, drug-eluting stents (DES) were introduced as a strategy to decrease restenosis and need for re-intervention. As the utilization of DES grew in general practice, there was considerable use of DES in "off-label" patients not evaluated in the initial randomized clinical trials. Single-center and large registry studies were able to demonstrate that the clinical efficacy of DES persisted even in patient subgroups not included in the initial clinical trials. These observations provided support for evaluating DES in STEMI patients. We will consider the evidence that evaluates the relative safety and efficacy of DES compared to BMS in STEMI patients, as well as address practical issues faced in the routine clinical care of these patients.

Assessment of coronary arterial restenosis with phase-contrast magnetic resonance imaging measurements of coronary flow reserve.

BACKGROUND: After successful percutaneous coronary arterial revascularization, 25% to 60% of subjects have restenosis, a recurrent coronary arterial narrowing at the site of the intervention. At present, restenosis is usually detected invasively with contrast coronary angiography. This study was performed to determine if phase-contrast MRI (PC-MRI) could be used to detect restenosis noninvasively in patients with recurrent chest pain after percutaneous revascularization. METHODS AND RESULTS: Seventeen patients (15 men, 2 women, age 36 to 77 years) with recurrent chest pain >3 months after successful percutaneous intervention underwent PC-MRI measurements of coronary artery flow reserve followed by assessments of stenosis severity with computer-assisted quantitative coronary angiography. The intervention was performed in the left anterior descending coronary artery in 15 patients, one of its diagonal branches in 2 patients, and the right coronary artery in 1 patient. A PC-MRI coronary flow reserve value /=70% and >/=50%, respectively. CONCLUSIONS: Assessments of coronary flow reserve with PC-MRI can be used to identify flow-limiting stenoses (luminal diameter narrowings >70%) in patients with recurrent chest pain in the months after a successful percutaneous intervention.

Visualization and functional assessment of proximal and middle left anterior descending coronary stenoses in humans with magnetic resonance imaging.

BACKGROUND: Coronary artery bypass grafting improves survival in patients with >70% luminal diameter narrowing of the 3 major epicardial coronary arteries, particularly if there is involvement of the proximal portion of the left anterior descending (LAD) coronary artery. Measurement of coronary flow reserve can be used to identify functionally important luminal narrowing of the LAD artery. Although magnetic resonance imaging (MRI) has been used to visualize coronary arteries and to measure flow reserve noninvasively, the utility of MRI for detecting significant LAD stenoses is unknown. METHODS AND RESULTS: Thirty subjects (23 men, 7 women, age 36 to 77 years) underwent MRI visualization of the left main and LAD coronary arteries as well as measurement of flow in the proximal, middle, or distal LAD both at rest and after intravenous adenosine (140 microgram/kg per minute). Immediately thereafter, contrast coronary angiography and when feasible, intracoronary Doppler assessments of coronary flow reserve, were performed. There was a statistically significant correlation between MRI assessments of coronary flow reserve and (a) assessments of coronary arterial stenosis severity by quantitative coronary angiography and (b) invasive measurements of coronary flow reserve (P<0.0001 for both). In comparison to computer-assisted quantitative coronary angiography, the sensitivity and specificity of MRI for identifying a stenosis >70% in the distal left main or proximal/middle LAD arteries was 100% and 83%, respectively. CONCLUSIONS: Noninvasive MRI measures of coronary flow reserve correlated well with similar measures obtained with the use of intracoronary Doppler flow wires and predicted significant coronary stenoses (>70%) with a high degree of sensitivity and specificity. MRI-based measurement of coronary flow reserve may prove useful for identification of patients likely to obtain a survival benefit from coronary artery bypass grafting.

Transluminal extraction catheter atherectomy followed by immediate stenting in treatment of saphenous vein grafts.

OBJECTIVES: The purpose of this study was to evaluate the effectiveness of transluminal extraction catheter (TEC) atherectomy followed by immediate Palmaz-Schatz coronary stenting of coronary bypass vein grafts. BACKGROUND: Degeneration of saphenous vein coronary bypass grafts has become a common problem. Repeat bypass surgery is associated with greater risk and a poorer outcome than the initial operation. Moreover, percutaneous interventional procedures in vein grafts have been associated with high procedural complication rates, including distal embolization, and high restenosis rates. TEC atherectomy may reduce distal embolization, and stenting may reduce restenosis rates. METHODS: We evaluated the procedural, hospital and clinical outcomes of TEC atherectomy followed by immediate Palmaz-Schatz coronary stenting of 53 vein grafts in 49 consecutive patients. The strategy was to limit instrumentation to extraction debulking and to stabilizing the site with stent deployment before using balloon dilation for optimal gain in lumen diameter. RESULTS: Results are shown as mean value (95% confidence interval [CI]). The mean graft age was 9.2 years (95% CI 7.9 to 10.5), and 1.0 (95% CI 1 to 1) TEC cutter (2.2 mm [95% CI 2.1 to 2.3]) and 1.7 (95% CI 1.4 to 2.0) Palmaz-Schatz coronary stents/ vein graft were used. The procedural success rate was 98%, with a minimal lumen diameter at baseline of 1.3 mm (95% CI 1.1 to 1.5), increasing to 3.9 mm (95% CI 3.6 to 4.2) (p < 0.05) after the TEC-stent procedure. Procedural complications occurred infrequently: graft perforation in 1 (2%) of 53 patients and distal embolization in 1 (2%) of 53 (same patient). In-hospital complications included non-Q wave myocardial infarction in two patients and death after a successful procedure in three (6%) (n = 1 each: massive bleeding from the catheter site; sepsis; and acute myocardial infarction with asystole in the distribution of the stented vessel). The event-free survival rate to hospital discharge was 90%. Clinical follow-up (13 months [95% CI 11 to 15]) was available for all patients. There were five (11%) revascularization procedures (three bypass grafts and two percutaneous transluminal coronary interventions), four (9%) nonfatal myocardial infarctions and five (11%) deaths, for a cumulative rate of 28% for any adverse outcome occurring in 13 of 46 patients. CONCLUSIONS: TEC atherectomy followed by immediate Palmaz-Schatz coronary stenting of stenoses in old (> 9 years) saphenous vein grafts can be successfully performed, with a low incidence of procedural and hospital complications. Clinical restenosis rates are low and less than those previously reported; however, late morbid cardiac events are still frequent in this high risk group of patients. These observational findings suggest that this technique may improve percutaneous management of vein graft disease, but optimal long-term management strategies remain to be determined.

Alteration of autonomic influence on left ventricular contractility by epicardial superfusion with hexamethonium and procaine.

OBJECTIVE: Since portions of autonomic nerves and receptors are located superficially on the heart, it is possible that neuromodulatory substances in pericardial fluid may modulate cardiac contractile function by altering autonomic neurotransmission. The aim of the study was to examine this hypothesis in anaesthetised dogs instrumented to measure left ventricular pressure and volume (conductance catheter). METHODS: The effects of electrical stimulation of cardiac sympathetic efferents in the ansa subclavia (n = 6), or parasympathetic efferents in the vagus (n = 6), on left ventricular contractility were evaluated during epicardial superfusion with Tyrode solution, or Tyrode solution containing hexamethonium (1 x 10(-4) M), or procaine (2%). The slope of the end systolic pressure-volume relationship (Ees), a load independent measure of left ventricular contractility, and the position of the relationship (Vmid) were obtained by rapid transient vena caval occlusion. RESULTS: Ansa subclavia stimulation increased Ees from 4.8(SD 1.8) to 8.3(3.0) mm Hg.ml-1 (p < 0.05), and Vmid shifted to the left, from 9(10) to 0(16) ml (p < 0.05). This response was abolished by epicardial superfusion with procaine, but not with hexamethonium. Vagal stimulation decreased Ees from 13.3(7.4) to 6.3(4.2) mm Hg.ml-1 (p < 0.05) and Vmid shifted to the right, from 12(10) to 18(8) ml (p < 0.05). These changes were abolished by both procaine and hexamethonium. Procaine did not affect the positive inotropic response to intravenous noradrenaline nor the cardiac depressor response to intravenous methylcholine, indicating that the myocardial contractile response was intact during epicardial superfusion with procaine. CONCLUSIONS: Neuromodulatory substances in the pericardial space may alter left ventricular contractility by modifying cardiac efferent autonomic neurotransmission on the epicardial surface of the heart.

Usefulness of two-dimensional echocardiography during low-level exercise testing early after uncomplicated acute myocardial infarction.

To determine whether 2-dimensional (2-D) echocardiographic measures of segmental and global left ventricular (LV) function immediately on recovery of low-level, symptom-limited treadmill exercise are as sensitive as the same variables measured at peak bicycle exercise, 21 patients were studied after acute myocardial infarction (AMI). The recovery treadmill ejection fraction analysis was predictive of the peak bicycle results in 18 of the 21 patients (86%) and recovery treadmill wall motion abnormalities were predictive of the peak bicycle analysis in 17 (81%) (p less than 0.01). These data indicate that 2-D echocardiography during the immediate recovery phase of low-level postinfarction treadmill testing was as sensitive as the peak exercise assessment of segmental and global LV function. Accordingly, the predictive value of rest and recovery exercise measures were prospectively assessed in 67 patients during a mean follow-up interval of 11 months (range 3 to 24). Clinical characteristics and treadmill electrocardiographic findings did not identify the 16 of 67 patients (24%) who had new cardiac events (3 cardiac deaths, 8 recurrent AMIs and 6 coronary artery bypass graft operations). However, a decrease in recovery ejection fraction units of more than 10% was seen in 7 of these 16 patients (44%) with events, compared with only 4 of the 51 (13%) without events (p less than 0.002), and new or worsening wall motion abnormalities on exercise recovery were seen in 10 of the 16 patients (63%) with events, but in only 10 of the 51 (20%) without (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Role of plaque size and degree of stenosis in acute myocardial infarction.

Angiographically apparent coronary artery stenoses limit coronary flow, produce symptomatic ischemia, and can be targeted for revascularization. Severe stenoses are more likely to occlude than segments without significant stenoses. Coronary angiography underestimates the extent of coronary atherosclerosis. Arterial segments without severe stenoses are much more common, and their risk of occlusion is not zero. Thus, the majority of myocardial infarctions are due to occlusion of arteries that do not contain obstructive coronary stenoses. Consequently, coronary angiography is not able to accurately predict the site of a coronary artery occlusion that subsequently will produce myocardial infarction.

The underlying coronary lesion in myocardial infarction: implications for coronary angiography.

Myocardial infarction is usually caused by sudden thrombotic occlusion of a coronary artery at the site of a fissured atherosclerotic plaque. Recent evidence suggests that coronary angiography may be insensitive in detecting and quantitating atherosclerosis. Serial angiographic studies demonstrate that the majority of myocardial infarctions occur due to occlusion of arteries that previously did not contain angiographically significant (greater than 50%) stenoses. Similarly, quantitative angiography performed after thrombolytic therapy indicates that the coronary lesion underlying the clot is frequently not severely stenotic. Thus, an angiographically apparent stenosis is not necessary for the development of a thrombotic occlusion resulting in an MI. These observations suggest that coronary angiography does not accurately predict the site of a subsequent occlusion that will produce a myocardial infarction.

Severe right heart failure in a patient with Grave's disease.

This brief report presents a patient with isolated right heart failure and two rare underlying causes, hyperthyroidism and dysplastic tricuspid valve. Repair of the tricuspid valve and treatment of the hyperthyroidism were both essential for successful treatment of the right heart failure. Most important, recrudescence of hyperthyroidism in this patient was associated with reappearance of florid right heart failure. This report provides further information about a potential linkage of hyperthyroidism and severe right heart failure.

The effects of intracoronary adenosine on preconditioning during coronary angioplasty.

There is evidence that the first balloon inflation during coronary angioplasty provides a preconditioning stimulus leading to decreased ischemia during subsequent balloon inflations. Endogenous adenosine release may play a role in ischemic preconditioning. Therefore, intracoronary adenosine administration prior to the first balloon inflation during percutaneous transluminal coronary angioplasty (PTCA) might modify the preconditioning response to the first balloon inflation. Forty-one patients underwent double-blind randomization to treatment with 100 mcg of intracoronary adenosine or placebo prior to coronary angioplasty. Twenty patients (11 adenosine, 9 placebo) had complete resolution of ischemia between inflations allowing comparison between the first and second inflation. An angioplasty guidewire was used to obtain an intracoronary electrocardiogram. The mean reduction in ST elevation during the second inflation compared with the first was 4.8 mm in the placebo group and -0.8 in the adenosine group (p < 0.05 placebo vs. adenosine). Seven of 9 placebo patients had a decrease in ischemia during the second inflation compared with the first, while only 2 of 11 adenosine patients showed a reduction. It was concluded that (1) the first inflation during PTCA is a preconditioning stimulus leading to a decrease in ischemia during later inflations, and (2) intracoronary adenosine administration prior to PTCA modifies the preconditioning effect of the first inflation. These data suggest that adenosine plays a role in ischemic preconditioning in humans.

Diagnosis and management of ischemic heart disease in the patient scheduled to undergo electroconvulsive therapy.

The cardiovascular risk of electroconvulsive therapy (ECT) is a product of the stress of ECT itself and the severity and stability of coronary artery disease (CAD), as well as other cardiovascular factors. ECT itself represents a relatively low-risk procedure. Patient-specific risk can be defined by a combination of clinical evaluation and noninvasive testing, much of which is aimed at detecting the presence and staging the severity and stability of CAD. Patients at high risk of a cardiac complication include those with severe or unstable symptoms of CAD, and they should undergo extensive cardiac evaluation before ECT Patients at low risk likely need no further evaluation and can undergo ECT. Patients at intermediate risk should have careful clinical evaluation, and most likely noninvasive evaluation, which should include some form of stress testing. Medical therapy should be continued and/or maximized in all patients with CAD. It is expected that with careful screening, patients with established CAD can undergo ECT safely.

Load dependence of left ventricular diastolic pressure-volume relations during short-term coronary artery occlusion.

We evaluated the effect of altered loading conditions on left ventricular (LV) diastolic pressure-volume relations during acute coronary artery occlusion that was produced by inflation of an intracoronary balloon. Open-chest anesthetized dogs (n = 18) were instrumented so that LV pressure (micromanometer) and LV volume (conductance) could be measured without disturbing the pericardium. The effects of brief periods of occlusion (1-2 minutes) were assessed under steady-state conditions before and after dextran infusion with the pericardium present and absent and during vena caval occlusion. Under steady-state conditions before dextran infusion with the pericardium removed, at an LV end-diastolic pressure (EDP) of 8.4 +/- 1.4 mm Hg, occlusion resulted in a rightward shift in the diastolic portion of the LV pressure-volume loop (delta LVEDP, 2.7 +/- 2.3 mm Hg; delta LVEDV, 6.3 +/- 4.7 ml, both p less than 0.05 versus control). After dextran infusion (LVEDP, 20.9 +/- 6.0 mm Hg), occlusion resulted in a rightward and upward shift in the diastolic portion of the LV pressure-volume loop (delta LVEDP, 5.8 +/- 4.4 mm Hg; delta LVEDV, 4.2 +/- 3.0 ml, both p less than 0.05 versus control). At low cardiac volumes before dextran infusion, the intact pericardium did not affect the response to occlusion. By contrast, after dextran infusion in the presence of an intact pericardium, LVEDP significantly increased (delta, 6.4 +/- 3.6 mm Hg, p less than 0.05) but LVDEV did not (delta, 0.7 +/- 1.5 ml, p = NS). There was a parallel upward shift in the diastolic portion of the LV pressure-volume loop that was eliminated by removal of the pericardium. Thus, the change in LV diastolic pressure and volume during occlusion varied and depended on the baseline cardiac volume and presence of the pericardium. Before dextran infusion with the pericardium present and absent, coronary artery occlusion did not alter the LV diastolic chamber stiffness parameter, which was calculated from the diastolic interval of an averaged steady-state beat (0.040 +/- 0.019 versus 0.036 +/- 0.015 mm Hg/ml, p = NS). After dextran infusion with the pericardium present and absent, coronary artery occlusion increased the LV diastolic chamber stiffness parameter (0.057 +/- 0.034 and 0.074 +/- 0.034 mm Hg/ml, both p less than 0.05 versus controls, respectively). Vena caval occlusion eliminated the shifts in the diastolic portion of the LV pressure-volume loop with the pericardium present and absent.(ABSTRACT TRUNCATED AT 400 WORDS)

The effect of vagal stimulation on left ventricular systolic and diastolic performance.

Vagal stimulation (VS) decreases heart rate and alters the loading conditions of the left ventricle (LV). However, its effects on LV performance are not clearly defined. To evaluate the effects of VS on LV performance, 20 anesthetized open-chest dogs were instrumented to measure LV pressure (LVP) and volume. VS resulted in a decrease in the slope of the end-systolic pressure-volume relationship, without pacing and with pacing, after ansae subclaviae resection and after ansae subclaviae resection plus beta-adrenergic blockade. VS did not alter the time constant of isovolumic relaxation (tau) or the LV end-systolic pressure-tau relationship during vena caval occlusion. No change was noticed in the LV chamber stiffness constant without and with pacing. However, a significant increase in the LV filling fraction at one-third and one-half of diastole was observed. We examined the mechanism of this increase by examining the relationship of left atrial pressure (LAP) and LVP. VS increased mean LAP 44% and increased the LAP-LVP gradient 42%. These data suggest that VS exerts a significant negative inotropic effect that is independent of its bradycardiac effect and the level of sympathetic tone. Despite the absence of lusitropic effects of VS, early filling of the LV is augmented most likely as a result of an increase in LAP.

Effects of vasoactive intestinal peptide on myocardial performance.

It is now recognized that stimulation of the vagus releases both acetylcholine (ACh) and vasoactive intestinal peptide (VIP). Whereas ACh depresses cardiac function, recent data indicate that VIP may have a cardiostimulatory effect. Exogenously administered VIP appears to enhance left ventricular (LV) contractile function; however, whether endogenously released VIP alters LV performance is not known. Accordingly, we evaluated the effects of exogenous VIP and endogenously released VIP during vagal stimulation after muscarinic and beta-adrenergic blockade (VS-B) on LV performance using pressure-volume analysis. Eight anesthetized open-chest dogs instrumented to measure LV pressure and volume (conductance catheter) were pretreated with atropine (0.1 mg/kg) and propranolol (1 mg/kg). The cervical vagi were transected. Hemodynamic data were obtained at steady state and during transient vena caval occlusion. Exogenous intravenous VIP (0.05 microgram/kg-1 x min-1) increased HR minimally [2.1 +/- 0.9% increase; P = not significant (NS)] but significantly increased maximum first time derivative of left ventricular pressure (dP/dtmax; 29.4 +/- 19.9% increase; P < 0.05) and the slope of the end-systolic pressure-volume relation (Ees; 3.1 +/- 1.3 to 8.9 +/- 4.2 mmHg/ml; P < 0.05). Minimum first time derivative of left ventricular pressure (dP/dtmin) decreased 22 +/- 16.2% (P < 0.05), and the time constant of isovolumic relaxation (tau) decreased 38 +/- 18% (P < 0.05). During VS-B (20 Hz, 15 v, 5 min), HR increased significantly (98 +/- 11 to 130 +/- 26 beats/min; P < 0.05). Ees also increased significantly (3.3 +/- 1.6 vs. 5.2 +/- 2.8 mmHg/ml; P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Congestive heart failure: systolic and diastolic function.

There is increasing recognition that disorders of both left ventricular systolic and diastolic function can result in congestive heart failure. As such, consideration of both the filling and emptying characteristics of the left heart is needed to evaluate the hemodynamic abnormalities present in this syndrome. Considerations of the systolic (emptying) and diastolic (filling) pumping characteristics of the left heart also provides a conceptual basis to classify and understand the pathophysiology of congestive heart failure. In this context, systolic dysfunction can be defined as impaired emptying of the LV, apparent as a decreased (< 50%) effective ejection fraction (forward stroke volume divided by end-diastolic volume). Systolic dysfunction may result from impaired myocardial contractile function, increased left ventricular afterload, and/or structural abnormalities of the left heart. Diastolic dysfunction can be defined as a condition in which filling of the LV sufficient to produce an adequate cardiac output requires an elevated pulmonary venous pressure. Thus, diastolic dysfunction is clinically manifested as pulmonary congestion. Defined in this manner, the most common cause of diastolic dysfunction is systolic dysfunction. In fact, the most common symptom of patients with systolic dysfunction is dyspnea from the resulting diastolic dysfunction. Diastolic dysfunction in the setting of normal systolic function may be due to obstruction of left ventricular filling, impaired left ventricular distensibility, or extensive external compression of the LV. Treatment of diastolic dysfunction can be accomplished by relieving myocardial ischemia, improving systolic function, lowering arterial systolic pressure, and decreasing cardiac distention.