Optimizing stent expansion with new stent delivery systems.

OBJECTIVES: The purpose of this study was to assess whether the newer stent delivery systems provide a stented lumen cross-sectional area (CSA) that is equal to the delivery balloon nominal dimensions. BACKGROUND: First generation stents were often not adequately expanded with their delivery system and frequently required higher pressure or a larger balloon after deployment. Newer stents were designed to optimize expansion with noncompliant, high-pressure balloons provided as the delivery systems. METHODS: Intravascular ultrasound (IVUS) was used to evaluate 38 stents in 32 patients after deployment at 14 to 16 atm with their delivery balloon system. Minimum stent lumen CSA and stent minimum lumen diameter (MLD) were measured by IVUS imaging. The manufacturer's expected stent diameter was defined as the balloon diameter measured by the company at the maximum pressure used. The manufacturer's expected stent area was calculated based on the manufacturer's expected stent diameter. RESULTS: The MLD (2.5 +/- 0.5 mm) and minimum stent CSA (6.0 +/- 1.7 mm(2)) by IVUS were significantly smaller than the manufacturer's expected stent diameter (3.5 +/- 0.4 mm) and area (9.5 +/- 1.9 mm(2)) (p < 0.0001, respectively). The mean MLD by IVUS was 72 +/- 8% of the expected stent diameter, and the mean minimum stent CSA by IVUS was 62 +/- 10% of the expected stent area. CONCLUSIONS: Despite moderately high-pressure inflations, the mean minimum stent CSA actually achieved was, on average, only 62% of the manufacturer's expected stent area. To optimize stent deployment, these IVUS observations should be considered during coronary artery stenting.

Does use of intravascular ultrasound accelerate arteriopathy in heart transplant recipients?

BACKGROUND: Intravascular ultrasound (IVUS) is a sensitive method for assessing allograft vasculopathy in heart transplant recipients, but it is not known whether this instrumentation traumatizes the transplanted arteries and affects progression of arteriopathy. METHODS AND RESULTS: Yearly coronary angiograms were obtained in 86 patients who underwent heart transplantation between January 1991 and May 1995. Patients were divided into 3 groups: (1) no IVUS performed after transplantation (group 1, n = 47); (2) IVUS of the left anterior descending artery (LAD) performed only at year 1 (group 2, n = 13); and (3) IVUS of the LAD performed at both baseline (within 2 months after transplantation) and year 1 after transplantation (group 3, n = 26). Coronary angiography measurements of lumen diameter were performed at 5 segments along the length of the LAD and left circumflex artery (LCX) from baseline through the second-year studies except in group 2, which did not receive a baseline angiogram; IVUS measurements were obtained at 10 cross sections from each artery. At baseline, there was no significant difference in vessel diameter for either the LAD or the LCX artery between the IVUS (group 3) and no IVUS (group 1) groups. Within each group, the lumen of both the LAD and LCX narrowed from baseline to year 1 (group 1: 3.3 +/- 0.6 mm to 2.8 +/- 0.5 mm in LAD, P =.001; 3. 3 +/- 0.6 mm to 3.0 +/- 0.5 mm in LCX, P =.006; group 3: 3.5 +/- 0.7 mm to 3.1 +/- 0.6 mm in LAD, P =.01; 3.1 +/- 0.6 mm to 2.8 +/- 0.5 mm in LCX, P = 0.07), but there were no significant differences between the instrumented artery (LAD) and control artery (LCX) or further changes observed at year 2. There were also no significant differences in the percent reductions at year 1 and year 2 between arteries or between groups. By IVUS, from baseline to year 1 in group 3, the plaque cross-sectional area (CSA) increased (1.6 +/- 1. 9 to 2.3 +/- 1.7 mm(2), P <.0001), the lumen CSA decreased (12.7 +/- 3.7 to 11.7 +/- 3.3 mm(2), P =.04), and the maximum lumen diameter decreased (4.2 +/- 0.6 to 4.0 +/- 0.6 mm, P =.04). CONCLUSIONS: The use of IVUS is not associated with acceleration of arteriopathy in heart transplantation recipients. Luminal narrowing occurs predominantly during the first year after transplantation. There was no significant change in lumen dimensions during the second year.

Comparison of the sheath delivery system versus bare stenting for coronary stent implantation.

Outside the United States, Palmaz-Schatz coronary stents are implanted by hand-crimping the stent to a high pressure balloon without the use of a protective sheath. This lowers the delivery profile, increases the ease of deployment, and ensures that the postdilatation balloon is centered on the stent. To assess this bare stenting technique, 209 patients were retrospectively analyzed: 92 patients (107 lesions) with the sheath protected stent delivery system (SDS) and 117 patients (150 lesions) with the bare stent approach. The number of balloons used per lesion in the bare stent group was significantly less than in the SDS group (1.9 +/- 0.6 vs. 3.8 +/- 1.2, P < 0.0001). In addition, the procedure time in the bare stent group was significantly shorter than in the SDS group (106 +/- 55 vs. 134 +/- 60 min, P = 0.001). There was no difference in frequency of adverse events or stent displacement during the procedure. The bare stenting technique decreases the procedure time, reduces the number of balloons used, and is as safe as the SDS approach.

Simultaneous measurement of myocardial oxygen consumption and blood flow using [1-carbon-11]acetate.

UNLABELLED: [1-Carbon-11]acetate has been used as a tracer for oxidative metabolism with PET. The aim of this study was to validate, in humans, a previously proposed two-compartment model for [1-11C]acetate for the noninvasive measurement of myocardial oxygen consumption (MVO2) and myocardial blood flow (MBF) with PET. METHODS: Twelve healthy volunteers were studied with [13N]ammonia, [1-11C]acetate and PET. Myocardial oxygen consumption was invasively determined by the Fick method from arterial and coronary sinus O2 concentrations and from MBF obtained by [13N]ammonia PET. RESULTS: Directly measured MVO2 ranged from 5.2 to 11.1 ml/100g/min, and MBF ranged from 0.48 to 0.88 ml/g/min. Oxidative flux through the tricarboxylic acid cycle, reflected by the rate constant k2, which correlated linearly with measured MVO2 [k2 = 0.0071 + 0.0074(MVO2); r = 0.74, s.e.e. = 0.015]. With this correlation, MVO2 could be estimated from the model-derived k2 value by MVO2 = 135(k2) - 0.96. The slope of this relationship was close to that previously obtained in rats and implies that the tricarboxylic acid cycle intermediate metabolite pool sizes are comparable. The net extraction (K1) of [1-11C]acetate, measured by PET, from blood into myocardium correlated closely with MBF by K1 = 0.15 + 0.73(MBF) (r = 0.93, s.e.e. = 0.033) and, thus, provided noninvasively obtainable measures of blood flow. CONCLUSION: The proposed compartment model for [1-11C]acetate fits the measured kinetics well and, with proper calibration, allows estimation of absolute MVO2 rather than only an index of oxidative metabolism. Furthermore, [1-11C]acetate-derived estimates of MBF are feasible.

Intravascular ultrasound identification of stent entrapment in vivo with in vitro confirmation.

OBJECTIVES: One potential complication of stenting is "stent jail" due to placement of a stent across a side branch, which may impede additional interventions. Another form of stent entrapment may occur if the guidewire is accidentally withdrawn and then unknowingly passes through a stent loop during reentry with subsequent high pressure expansion. The purpose of this study was to evaluate this form of stent entrapment in vitro by intravascular ultrasound (IVUS). METHODS: A guidewire was passed through the end or middle diamonds of Palmaz-Schatz and Palmaz stents or the middle of Gianturco-Roubin stents. A 3.5 mm balloon was inflated over the guidewire through the various side holes of the stents. RESULTS: IVUS images presented three distinct patterns depending on the type of stent and position of balloon entry: 1) external compression and loss of wall continuity in the Palmaz-Schatz and Palmaz stents, 2) displacement of the side diamond across the lumen, and 3) external compression of the Gianturco-Roubin stent. The first and second patterns but not the third one were associated with impairment of lumen access. CONCLUSIONS: Based upon this in vitro verification, IVUS imaging can be used to identify the presence of stent entrapment in vivo.

Transesophageal echocardiography during radiofrequency catheter ablation of ventricular tachycardia.

Radiofrequency lesion formation requires stable catheter tip/endocardial contact. Energy delivery is limited when temperatures are > 100 degrees C due to coagulum formation at the catheter tip. Transesophageal echocardiographic imaging may be useful for monitoring catheter position and detecting boiling. Transesophageal echocardiographic images were recorded during production of 22 radiofrequency lesions in bovine myocardium in a saline bath. Lesion size, tissue temperature and appearance of echo contrast (bubbles) were assessed. In 11 patients, transesophageal echocardiography was used to guide catheter movement and detect boiling during radiofrequency ablation for ventricular tachycardia. In the tissue bath, the appearance of echo bubbles was associated with visual bubbling at the catheter tip, tissue temperatures > 60 degrees C and larger lesions (284 +/- 165 vs 30 +/- 54 mm3; p < 0.001). In humans, transesophageal images easily identified the catheter tip in either ventricle and enabled continuous observation of electrode-tissue contact during radiofrequency application. Transesophageal echocardiographic bubbles appeared in 59 of 217 radiofrequency applications (27%). Continued radiofrequency application after appearance of bubbles was followed by an increase in impedance. Prolonged placement of the probe in heavily sedated patients resulted in a mild sore throat, but no other complications. Transesophageal echocardiographic imaging enables continuous monitoring of catheter position during radiofrequency energy application. The abrupt appearance of echo bubbles indicates boiling and impending coagulum formation at the catheter tip.

Ventricular tachycardia after infarction: sources of coronary blood flow to the infarct zone.

The purpose of this study was to determine the sources of coronary blood flow to infarct scars in patients with sustained ventricular tachycardia occurring late after myocardial infarction, which is necessary for transcoronary sclerosis or embolization. Angiograms of 32 consecutive patients (age 63 +/- 8 years, ejection fraction 0.30 +/- 0.10) were reviewed. Sources of blood flow to the infarct zone were identified as coming from a recanalized infarct-related artery, side branch, collateral, or coronary bypass graft. Eighty-four percent of patients in the study had an identifiable blood supply to the area of previous infarction. More than one source of blood flow to anterior infarct locations were observed more often than to inferior infarct locations (53% vs 17%, p = 0.03). Transcoronary mapping for possible chemical ablation should be technically feasible in the majority of patients with ventricular tachycardia. Infarct zone blood flow arises from any of several sources and varies somewhat depending on infarct location.

Metabolic and functional recovery of ischemic human myocardium after coronary angioplasty.

Although revascularization of hypoperfused but metabolically active human myocardium improves segmental function, the temporal relations among restoration of blood flow, normalization of tissue metabolism and recovery of segmental function have not been determined. To examine the effects of coronary angioplasty on 13 asynergic vascular territories in 12 patients, positron emission tomography and two-dimensional echocardiography were performed before and within 72 h of revascularization. Ten patients underwent late echocardiography (67 +/- 19 days) and eight underwent a late positron emission tomographic study (68 +/- 19 days). The extent and severity of abnormalities of wall motion, perfusion and glucose metabolism were expressed as wall motion scores, perfusion defect scores and perfusion-metabolism mismatch scores. Angioplasty significantly increased mean stenosis cross-sectional area (from 0.95 +/- 0.9 to 2.7 +/- 1.4 mm2) and mean cross-sectional luminal diameter (from 0.9 +/- 0.6 to 1.9 +/- 0.5 mm) (both p less than 0.001). Perfusion defect scores in dependent vascular territories improved early after angioplasty (from 116 +/- 166 to 31 +/- 51, p less than 0.002) with no further improvement on the late follow-up study. The mean perfusion-metabolism mismatch score decreased from 159 +/- 175 to 65 +/- 117 early after angioplasty (p less than 0.01) and to 26 +/- 29 at late follow-up (p less than 0.001 vs. before angioplasty; p = NS vs. early after angioplasty). However, absolute rates of glucose utilization remained elevated early after revascularization, normalizing only at late follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)

Programmed electrical stimulation at potential ventricular reentry circuit sites. Comparison of observations in humans with predictions from computer simulations.

The purpose of this study was to define specific types of resetting responses to programmed electrical stimulation during human ventricular tachycardia and to use computer simulations of reentry circuits to assess the possible mechanisms and pacing site location relative to the reentry circuit for each type of response. The effects of scanning single stimuli at 35 left ventricular endocardial sites during sustained monomorphic ventricular tachycardia in 12 patients were studied. In considering alterations in QRS configuration and the delay between the stimulus and the advanced QRS, we identified three types of resetting responses to scanning stimuli consistent with stimulation at sites in or near the reentry circuit at 12 abnormal endocardial sites in eight patients. Type 1: all capturing stimuli were followed after a delay by early QRS complexes that had the same configuration as the tachycardia complexes. Type 2: late stimuli reset tachycardia as in type 1 but early stimuli reset the tachycardia after altering the QRS configuration. Type 3: late stimuli reset tachycardia as in type 1, but early stimuli advanced tachycardia with a short stimulus to QRS delay without altering the QRS configuration. In the simulations, premature depolarization of sites in the circuit produced orthodromic and antidromic wavefronts. The orthodromic wavefront propagated through the circuit and exited the circuit at the same site as did the previous tachycardia wavefronts and advanced the tachycardia without altering the configuration of the advanced QRS. The antidromic wavefront of relatively late stimuli was confined within or near the circuit by collision with the orthodromic wavefront of the preceding tachycardia beat and failed to alter ventricular activation distant from the circuit. Therefore, the QRS configuration after the stimulus was unchanged. A type 1 response occurred when all capturing stimuli produced this effect. However, with increasing stimulus prematurity, the antidromic wavefront propagated farther before colliding with an orthodromic wavefront, and under some conditions, it exited the circuit from a site other than the original circuit "exit," and altered the ventricular activation sequence distant from the circuit and, therefore, the QRS configuration, producing a type 2 pattern. The type 3 pattern occurred when the antidromic wavefront of early premature beats captured the original circuit exit. The effect of a stimulus was dependent on the stimulus prematurity, the relative conduction times from the stimulation site to the potential sites of "exit" from the circuit, and the timing of the excitable gap at the stimulation site.(ABSTRACT TRUNCATED AT 400 WORDS)

The value of echocardiography in blunt chest trauma.

All victims of blunt injury to the chest or precordium admitted to a Level I trauma center in a 1-year period were evaluated prospectively with two-dimensional echocardiography on the day of admission, serial determinations of creatine kinase (CK) and MB isoenzyme radioimmunoassay (CK-MB) over the first 24 hours, continuous electrocardiographic monitoring over at least the first day, and serial 12-lead electrocardiography (ECG) over the first 3 days. The patients were divided into four groups based upon the results of echocardiography. Group A (n = 35) had normal ECHO and ECG; Group B (n = 16), normal ECHO and abnormal ECG; group C (n = 14), ECHO showing abnormal wall motion and/or pericardial fluid; group D (n = 8), ECHO showing a nontraumatic valvular or wall motion abnormality. Nineteen patients required an operation under general anesthesia. Group C patients had significantly higher CK, CK-MB, numbers of associated injuries, and Injury Severity Scores; seven required invasive hemodynamic monitoring. No cardiac morbidity of general anesthesia was seen. We conclude that echocardiography is an important tool for diagnosis and triage which may be used to stratify a homogeneous patient population into groups with acute, chronic, and no cardiac disease. Cardiac injury occurs in a setting of multisystem trauma. Patients with normal echocardiogram and ECG on admission do not require intensive care monitoring.

Silent ischemia during coronary occlusion produced by balloon inflation: relation to regional myocardial dysfunction.

Thirty patients with stable exertional angina undergoing percutaneous transluminal coronary angioplasty of an isolated obstructive lesion of the proximal left anterior descending artery were prospectively evaluated to investigate the relation between angina induced by balloon inflation and the quantity and severity of myocardial ischemia as determined by electrocardiographic (ECG) monitoring and by echocardiographic assessment of regional and global left ventricular wall motion. Anginal pain interviews, continuous two-dimensional echocardiographic recordings and 12 lead ECG recordings at 10 second intervals were obtained for the first two inflation sequences. Seventeen patients had angina with both inflations (symptomatic group), seven patients had no angina or related symptoms during either inflation (asymptomatic group) and six patients had both painful and painless inflations (mixed response group). Comparison of the three groups revealed that they did not differ in mean age, sex distribution, prior history of angina or the incidence of comorbid conditions. Echocardiographic measurements of global and regional left ventricular dysfunction during balloon inflation were comparable in the symptomatic and asymptomatic groups. Similarly, there were no significant differences in the time to onset or magnitude of ST segment changes. The results of the wall motion and ECG studies in the mixed response group paralleled the results in the symptomatic and asymptomatic groups, with no significant differences in any of the variables measured between the painful and painless inflations. These data demonstrate that silent myocardial ischemia occurs in an appreciable proportion of patients during coronary angioplasty and the absence of angina does not imply that a lesser amount of myocardium is jeopardized than with painful inflations.

Nontransmural myocardial infarction: a comparison of hospital and late clinical course of patients with that of matched patients with transmural anterior and transmural inferior myocardial infarction.

The hospital and long-term course of 67 patients with nontransmural myocardial infarction was compared with that of 66 patients with transmural anterior and 63 patients with transmural inferior infarction matched for age, sex, previous infarction and prior congestive heart failure. During their hospital stay, patients with nontransmural infarction had significantly less congestive heart failure and fewer intraventricular conduction defects than did patients with transmural anterior infarction; fewer atrial tachyarrhythmias and less sinus bradycardia and atrioventricular block than did patients with transmural inferior infarction; and an incidence of hypotension, pericarditis and ventricular irritability similar to that of patients in the other two groups. Patients with nontransmural infarction had a significantly lower coronary care unit mortality rate (9 percent) than that of patients with transmural anterior or transmural inferior infarction (20 and 19 percent, respectively). By 3 months, the mortality rate had risen to 14 percent in patients with nontransmural infarction, but was significantly higher (29 and 27 percent, respectively) in patients with transmural anterior or transmural inferior infarction. Angina was common in all three groups, occurring in more than 50 percent of patients during a mean follow-up period of 28.6 months after hospital discharge. In contrast, the incidence of subsequent myocardial infarction was significantly greater in patients with nontransmural myocardial infarction, occurring in 21 percent at 9 months compared with only 3 percent of patients with transmural anterior (p less than 0.01) and 2 percent of patients with transmural inferior (p less than 0.05) infarction. By 54 months, 57 percent of patients with nontransmural infarction had sustained a new infarction contrasted with only 12 percent of patients with transmural anterior (p less than 0.001) and 22 percent of patients with transmural inferior (p less than 0.01) infarction. Late mortality increased in patients with nontransmural myocardial infarction and, although this group had a significantly better survival rate at 3 months, the overall late mortality of the three groups was comparable. The study suggests that nontransmural myocardial infarction is an unstable ischemic event associated with a great risk of later myocardial infarction and high late mortality rate. A more aggressive diagnostic and therapeutic approach may be warranted in patients with nontransmural myocardial infarction.

Coronary arterial spasm versus esophageal spasm. Response to ergonovine.

In this report we show that coronary arterial and esophageal spasm are sometimes clinically indistinguishable. Pain patterns can be identical, nitroglycerin can bring relief, interval electrocardiograms and exercise electrocardiograms generally disclose no abnormalities, coronary arteriograms may be within normal limits or nearly so, and, importantly, an ergonovine provocative test can provoke esophageal spasm accompanied by pain mistaken for Prinzmetal's angina. Accordingly, chest pain in response to the administration of ergonovine is not evidence of coronary arterial spasm without simultaneous arteriographic proof together with changes in the monitoring electrocardiogram. Conversely, gastroenterologists should not expose patients to the risk of ergonovine without prior assurance that the coronary arterial response is normal. Our observations illustrate these points and identify a patient with symptomatic esophageal spasm previously diagnosed as Prinzmetal's angina.