Gastrointestinal complications in heart transplant patients: MITOS study.

INTRODUCTION: The most frequent immunosuppressive treatment complications in solid organ transplant recipients are gastrointestinal (GI) disorders. MATERIALS AND METHODS: An observational, cross-sectional study to evaluate the prevalence and management of GI complications in transplanted patients was conducted via a written questionnaire given to doctors at their practice. RESULTS: This study included 1788 patients; 181 corresponded to heart transplant recipients. The mean age for the heart transplant patients was 58.7 +/- 11.8 years. The mean time from the transplantation was 5.2 +/- 4.4 years. GI complications were seen in 38.7% of cases. Regarding the clinical management, in 72.9% of cases patients with GI complications received pharmacologic treatment, 86.3% with gastric protectors, 32.8% reduced the dose of some drug, 8.1% interrupted the drug temporarily, and 10.9% discontinued the drug permanently. The drug that was always discontinued was mycophenolate mofetil (MMF), and in 85.7% of cases in which the dose of an immunosuppressive drug was reduced, the reduced drug was also MMF. CONCLUSIONS: Almost 40% of heart transplant recipients suffered GI complications which affected daily activities in most cases. The most used strategy to manage these complications was based on a treatment with gastric protectors together with dose reduction and/or partial or definitive MMF discontinuation.

Impact of atrioventricular compliance on pulmonary artery pressure in mitral stenosis: an exercise echocardiographic study.

BACKGROUND: The decay of the pressure gradient across a stenotic mitral valve is determined by the size of the orifice and net AV compliance (C(n)). We have observed a group of symptomatic patients, usually in sinus rhythm, characterized by pulmonary hypertension (particularly during exercise) despite a relatively large mitral valve area by pressure half-time. We speculated that this discrepancy was due to low atrial compliance causing both pulmonary hypertension and a steep decay of the transmitral pressure gradient despite significant stenosis. We therefore tested the hypothesis that C(n) is an important physiological determinant of pulmonary artery pressure at rest and during exercise in mitral stenosis. METHODS AND RESULTS: Twenty patients with mitral stenosis were examined by Doppler echocardiography. C(n), calculated from the ratio of effective mitral valve area (continuity equation) and the E-wave downslope, ranged from 1.7 to 8.1 mL/mm Hg. Systolic pulmonary artery pressure (PAP) increased from 43+/-12 mm Hg at rest to 71+/-23 mm Hg (range, 40 to 110 mm Hg) during exercise. There was a particularly close correlation between C(n) and exercise PAP (r=-0.85). Patients with a low compliance were more symptomatic (P<0.025). Catheter- and Doppler-derived values for C(n), determined in 10 cases, correlated well (r=0.79). CONCLUSIONS: C(n), which can be noninvasively assessed, is an important physiological determinant of PAP in mitral stenosis. Patients with low C(n) represent an important clinical entity, with symptoms corresponding to severe increases in PAP during stress echocardiography.

Bradyarrhythmias: clinical significance and management.

Clinicians have long recognized the potentially serious manifestations of extreme bradycardia. However, even marked bradycardia can often be physiologic, and in the presence of impaired ventricular function may offer important compensatory hemodynamic effects. Disorders of the sinoatrial node producing bradycardia include failure of impulse formation, sinoatrial conduction block, concealed sinus-perinodal reentry, carotid sinus hypersensitivity and the constellation of brady- and tachyarrhythmias that compose the "sick sinus syndrome." Bradycardia can also result from intraatrial block, atrioventricular nodal block or infranodal block. In addition, paroxysmal supraventricular tachyarrhythmias may produce concealment into the atrioventricular junction and simultaneous suppression of sinus node rhythmicity, resulting in long pauses. Pseudobradycardias manifesting as slow peripheral pulse rates can result from frequent, nonconducted early atrial premature beats, from ventricular bigeminy or runs of ventricular extrasystoles or from mechanical alternans. Cardiac pacemakers play an important role in the management of patients with severe symptoms attributable to bradyarrhythmias. However, excessive use of pacemakers and the inappropriate selection of physiologically unfavorable pacemaker systems should be avoided. Frequently, patients who are only mildly symptomatic with bradycardia should not receive a cardiac pacemaker because the prognosis is favorable. Patients with the tachy-bradycardia syndrome often require both pharmacologic and pacemaker therapy. In selected patients electrophysiologic testing may be helpful, but the majority of patients are best managed by careful attention to the history, electrocardiogram and ambulatory electrocardiographic recordings.

Shortened Doppler-derived mitral A wave deceleration time: an important predictor of elevated left ventricular filling pressure.

OBJECTIVES: The aim of this study was to investigate whether a new variable of mitral inflow, A wave deceleration time, identifies patients with elevated left ventricular filling pressures. BACKGROUND: In patients with an elevated left ventricular end-diastolic pressure, the increase in left ventricular pressure after atrial contraction rapidly exceeds left atrial pressure, resulting in abrupt cessation of the A wave. Therefore, we postulated that a shortening of A wave deceleration time might be a marker for elevated end-diastolic pressure. METHODS: Adequate pulsed Doppler mitral inflow velocities could be recorded in 40 of 44 consecutive patients undergoing cardiac catheterization with capillary wedge pressure in 20 patients, and within 1 h after left ventricular end-diastolic pressure recording in 20. Fifteen healthy volunteers were also studied. RESULTS: Left ventricular end-diastolic pressure was 8 to 35 mm Hg, and mean pulmonary wedge pressure was 6 to 37 mm Hg. Close correlations were found between A wave deceleration time and mean pulmonary wedge pressure (r = -0.87) and left ventricular end-diastolic pressure (r = -0.74). There were modest correlations between both pressures and peak E/A, E wave deceleration time and A wave duration, respectively; r = 0.59, -0.30 and -0.58 for capillary wedge and r = 0.25, -0.38 and -0.49 for end-diastolic pressures. A wave deceleration time 18 mm Hg, respectively, with a sensitivity of 67% and 89% and specificity of 100% for both. CONCLUSIONS: A shortened Doppler mitral inflow A wave deceleration time is a useful index of elevated left ventricular filling pressure.

Prediction of immediate ventricular arrhythmias after coronary artery ligation.

OBJECTIVES: Our aim was to test the hypothesis that increased beat to beat morphologic variations in the body surface electrocardiogram (ECG) are associated with fragmented diastolic electrical activity that appears after coronary artery ligation and to correlate the appearance of spontaneous ventricular fibrillation after coronary ligation with the magnitude of the ECG beat to beat variability. BACKGROUND: Unstable and variably delayed electrical activation precedes the development of ventricular fibrillation in dogs with acute ischemia. Detection of these highly variable low amplitude signals from the body surface is currently impossible. We have developed a system designed to measure the degree of beat to beat variability of the ECG. METHODS: With high fidelity electrocardiography, subtle beat to beat ECG morphologic variations were detected in epicardial and body surface electrograms and quantified as the variance of the ECG voltage at specific points of the cardiac cycle. The ratio of the variance at the QRS offset to that of the QRS onset (beat to beat variability index) was then calculated. RESULTS: Ventricular fibrillation developed in 12 of 27 dogs after left anterior descending coronary artery ligation. In 7 of the 12 dogs it occurred immediately (< 15 min) after ligation; in the other 5 it developed late (> 15 min) after ligation. Dogs with subsequently immediate ventricular fibrillation had a significantly higher beat to beat variability index than that of dogs with late or no ventricular fibrillation both before coronary ligation (4.7 +/- 1.4 vs. 1.1 +/- 0.2 and 0.8 +/- 0.1, respectively, p < 0.001) and after ligation (6.4 +/- 2.6, 1.0 +/- 0.6 and 1.2 +/- 0.6, respectively, p < 0.001). In dogs that developed ventricular fibrillation immediately after coronary ligation, the arrhythmia was preceded by fragmented diastolic electrical activity on the epicardial electrogram and a simultaneous increase in the beat to beat morphologic variability of the terminal portion of the body surface ECG QRS complex. CONCLUSIONS: Beat to beat QRS offset morphologic variations appear to be increased before and further increased after coronary artery ligation in dogs that develop ventricular fibrillation immediately after ligation. Increased beat to beat variability index may be associated with the presence of electrophysiologic instability and can predict early ventricular fibrillation.

Additional ST segment elevation during the first hour of thrombolytic therapy: an electrocardiographic sign predicting a favorable clinical outcome.

OBJECTIVES: The aim of this study was to investigate the significance of further ST elevation that occurs during the 1st h of thrombolytic therapy before the expected resolution. BACKGROUND: Early resolution of ST segment elevation is commonly accepted as a marker of clinical reperfusion during thrombolytic therapy for acute myocardial infarction. Using frequent electrocardiographic recordings, we observed in some patients further ST elevation that occurred during hour 1 of thrombolysis before the expected resolution. METHODS: To investigate the significance of this pattern, we classified 177 consecutive patients with a first acute myocardial infarction into two groups: Group A, 98 patients with ST elevation > or = 1 mm above the initial ST elevation during the 1st h of thrombolytic therapy, and Group B, 79 patients without this finding. RESULTS: Although the presence or absence of additional ST elevation was not associated with a clinical or prognostic difference in patients with a first inferior or posterior acute myocardial infarction, its presence indicated a more favorable clinical outcome and prognosis in patients with anterior infarction. Among the patients with anterior infarction the 65 patients in Group A had a higher ejection fraction (44 +/- 9% vs. 35 +/- 11%, p < 0.01), less heart failure (15% vs. 35%, p = 0.02) and a lower in-hospital mortality rate (0% vs. 8%, p = 0.04) than did the 37 patients from Group B. CONCLUSIONS: Additional ST elevation early during thrombolytic therapy in patients with anterior infarction suggests a favorable clinical outcome and thus may be indicative of successful reperfusion.

Acute myocardial infarction with isolated ST-segment elevation in posterior chest leads V7-9: "hidden" ST-segment elevations revealing acute posterior infarction.

OBJECTIVES: This study was done to determine whether electrocardiographic (ECG) isolated ST-segment elevation (ST) in posterior chest leads can establish the diagnosis of acute posterior infarction in patients with ischemic chest pain and to describe the clinical and echocardiographic characteristics of these patients. BACKGROUND: The absence of ST on the standard 12-lead ECG in many patients with acute posterior infarction hampers the early diagnosis of these infarcts and thus may result in inadequate triage and treatment. Although 4% of all acute myocardial infarction (AMI) patients reveal the presence of isolated ST in posterior chest leads, the significance of this finding has not yet been determined. METHODS: We studied 33 consecutive patients with ischemic chest pain suggestive of AMI without ST in the standard ECG who had isolated ST in posterior chest leads V7 through V9. All patients had echocardiographic imaging within 48 h of admission, and 20 patients underwent coronary angiography. RESULTS: Acute myocardial infarction was confirmed enzymatically in all patients and on discharge ECG pathologic Q-waves appeared in leads V7 through V9 in 75% of the patients. On echocardiography, posterior wall-motion abnormality was visible in 97% of the patients, and 69% had evidence of mitral regurgitation (MR), which was moderate or severe in one-third of the patients. Four patients (12%), all with significant MR, had heart failure, and one died from free-wall rupture. The circumflex coronary artery was the infarct related artery in all catheterized patients. CONCLUSIONS: Isolated ST in leads V7 through V9 identify patients with acute posterior wall myocardial infarction. Early identification of those patients is important for adequate triage and treatment of patients with ischemic chest pain without ST on standard 12-lead ECG.

Extracellular potassium ion dynamics and ventricular arrhythmias in the canine heart.

The relation between extracellular potassium ion activity [( K+]o) and ventricular tachyarrhythmias was studied in an open chest canine model with the use of two protocols. In Protocol I, potassium chloride was administered into the proximal left anterior descending coronary artery at a rate of 0.125 mEq/min for either 20 min or until [K+]o = 20 mEq/liter, whichever came first. In Protocol II, the proximal left anterior descending coronary artery was occluded in one step and was reperfused 20 min later. Fifteen dogs were subjected to Protocol I, nine of which were also subjected to Protocol II. In the latter group, a recovery period of greater than or equal to 1 h separated the two protocols. Local K+ and intramyocardial activities were recorded with use of bifunctional ion-sensitive plunge electrodes at multiple sites located in the region of the left ventricle perfused by the left anterior descending artery and at one site outside of this region. The following variables were recorded and analyzed: Lead II electrocardiogram, heart rate, systemic arterial blood pressure, local [K+]o and its time derivative (dK+/dt), local electrograms and ventricular arrhythmias. Maximal [K+]o and dK+/dt were 23 +/- 3 mEq/liter and 9 +/- 1 mEq/liter per min in Protocol I and 14 +/- 1 mEq/liter and 3 +/- 1 mEq/liter per min in Protocol II, respectively. In both protocols, the occurrence of ventricular arrhythmias correlated with [K+]o (p less than 0.02) as well as with dK+/dt (p less than 0.05). Ventricular arrhythmias were more frequent and more severe in Protocol II than in Protocol I (p less than 0.05). Therefore, whereas K+ dynamics were more pronounced in Protocol I, ventricular arrhythmias were more severe in Protocol II. This occurrence was apparently due, at least in part, to less heterogeneous changes in K+ gradients during constant K+ infusion. It was concluded that, in addition to the magnitude of [K+]o, the rate of change of this variable (that is, dK+/dt) apparently plays an important role in the genesis of ischemic ventricular arrhythmias.

Experimental ultrasonic angioplasty: disruption of atherosclerotic plaques and thrombi in vitro and arterial recanalization in vivo.

To investigate the use of high energy ultrasound as an alternative energy for angioplasty, an experimental ultrasonic angioplasty device was developed. The device was studied in two bioassay systems: an in vitro system for the disruption of atherosclerotic plaques and thrombi and an in vivo system for the recanalization of occluded canine femoral arteries. In vitro, sonication efficiently reduced the size of the plaques. Atheromatous plaques (n = 11) disrupted at a rate of 21 +/- 8 s/cm2; complicated plaques (n = 14) disrupted at a rate of 132 +/- 45 s/cm2 (p less than 0.001). Histologic examination revealed that the disruption of the plaques took place without concurrent damage to the media or adventitia. Ninety percent of the disrupted plaque debris had a diameter of less than 20 microns and was composed primarily of cholesterol monohydrate crystals. Solid thrombus (n = 5) weight was reduced from 1.6 +/- 0.2 to 0.4 +/- 0.1 g (p less than 0.0001) after 20 s of sonication. In vivo, sonication resulted in recanalization in all seven arteries tested in seven dogs. The obstruction was reduced from 93 +/- 11% to 18 +/- 7% (p less than 0.001). On histologic examination, the arterial wall injury index was found to be 1.56 +/- 0.42 in the test arteries compared with 1.37 +/- 0.47 in the control arteries (p = NS). The disruption of atherosclerotic plaques and thrombi, together with the efficient recanalization of the occluded arteries, demonstrates the potential of ultrasound angioplasty as a catheter-based technique for angioplasty.(ABSTRACT TRUNCATED AT 250 WORDS)

Improved posterobasal segment function after thrombolysis is associated with decreased incidence of significant mitral regurgitation in a first inferior myocardial infarction.

OBJECTIVES: This study was designed to investigate the association between wall motion abnormalities and the occurrence of ischemic mitral regurgitation in patients with a first inferior or posterior myocardial infarction and to reassess the role of thrombolytic treatment in these patients. BACKGROUND: We previously demonstrated that thrombolytic therapy reduces the incidence of significant mitral regurgitation in patients with a first inferior myocardial infarction, but the mechanisms responsible for this decrease were not clear. METHODS: Wall motion score on two-dimensional echocardiography (16 segments) and mitral regurgitation grade (0 to 3) on Doppler color flow imaging were assessed in 95 patients (in 47 after thrombolysis) at 24 h, 7 to 10 days and 1 month after myocardial infarction. Significant mitral regurgitation was defined as moderate or severe (grade 2 or 3). RESULTS: Multivariate analysis revealed that the presence of an advanced wall motion abnormality of the posterobasal segment of the left ventricle was the most significant independent variable associated with significant mitral regurgitation: odds ratio (OR) 15.0, 90% confidence interval (CI) 1.4 to 165.6 at 24 h; OR 2.8, CI 0.9 to 9.3 at 7 to 10 days; OR 4.2, CI 1.2 to 11.4 at 1 month. Thrombolysis reduced the prevalence of advanced wall motion abnormalities in the posterobasal segment at 24 h (55% vs. 75%, OR 0.5, CI 0.2 to 0.99), 7 to 10 days (44% vs. 73%, OR 0.3, CI 0.1 to 0.7) and 1 month (36% vs. 56%, OR 0.4, CI 0.2 to 0.9). CONCLUSIONS: There is a strong association between advanced wall motion abnormalities in the posterobasal segment and significant mitral regurgitation. In this study group, thrombolysis reduced the prevalence of advanced wall motion abnormalities in the posterobasal segment and thereby reduced the incidence of significant mitral regurgitation.

Calcium channel blocking agents and risk of cancer in patients with coronary heart disease. Benzafibrate Infarction Prevention (BIP) Study Research Group.

OBJECTIVES: This analysis sought to estimate the risk ratio for cancer incidence and cancer-related mortality associated with the use of calcium channel blocking agents (CCBs) in a large group of patients with chronic coronary heart disease (CHD). BACKGROUND: Recent publications contend that the use of short-acting CCBs may double the risk of cancer incidence and possibly increase mortality in hypertensive patients. METHODS: Cancer incidence data were obtained for 11,575 patients screened for the Bezafibrate Infarction Prevention (BIP) study, one-half of whom were treated at the time of screening with CCBs, over a mean follow-up period of 2.8 years. Cause-specific mortality was available through September 1996 (mean follow-up 5.2 years). The statistical power of detecting an odds ratio > or = 1.5 (given the cancer incidence rate of 2.1 in the nonusers of CCBs) was 0.91. The power declined to 0.77, 0.54 and 0.41, with declining odds ratios of 1.4, 1.3 and 1.25, respectively. RESULTS: Of 246 incident cancer cases, 129 occurred among the users (2.3%) and 117 among nonusers of CCBs (2.1%). After adjustment for age, gender and smoking, the odds ratio estimates for all cancers combined was 1.07 (95% confidence interval [CI] 0.83 to 1.37) for CCB users relative to nonusers. The adjusted risk ratio for all-cause mortality for age, gender and smoking and pertinent prognostic clinical characteristics was estimated at 0.94 (95% CI 0.85 to 1.04). The adjusted risk ratio for cancer-related mortality was 1.03 (95% CI 0.75 to 1.41). CONCLUSIONS: Patients with CHD treated with CCBs exhibited a similar risk of cancer incidence and total and cancer-related mortality compared with nonusers of CCBs. This analysis provides a certain assurance that CCB use in middle-aged and elderly patients with CHD is not associated with a meaningful difference in cancer incidence and related mortality.

Significance of ST segment elevations in posterior chest leads (V7 to V9) in patients with acute inferior myocardial infarction: application for thrombolytic therapy.

OBJECTIVES: This study was designed to examine whether ST segment elevation in posterior chest leads (V7 to V9) during acute inferior myocardial infarction (MI) identifies patients with a concomitant posterior infarction and whether these patients might benefit more from thrombolysis. BACKGROUND: Because the posterior wall is faced by none of the 12 standard electrocardiographic (ECG) leads, the ECG diagnosis of posterior infarction is problematic and has often remained undiagnosed, especially in the acute phase. METHODS: Eighty-seven patients with a first inferior infarction who were treated with recombinant tissue-type plasminogen activator were stratified according to the presence (Group A [46 patients]) or absence (Group B [41 patients]) of concomitant ST segment elevation in posterior chest leads V7 to V9. RESULTS: Patients in Group A had a higher incidence of posterolateral wall motion abnormalities (p < 0.001) on radionuclide ventriculography, a larger infarct area (as evidenced by higher peak creatine kinase levels) (p < 0.02) and a lower left ventricular ejection fraction (LVEF) at hospital discharge (p < 0.008) than those in Group B. ST segment elevation in leads V7 to V9 was associated with a higher incidence of at least one of the following adverse clinical events: reinfarction, heart failure or death (p = 0.05). Although patency of the infarct-related artery (IRA) in Group A resulted in an improved LVEF at discharge (p < 0.012), LVEF was unchanged in Group B, regardless of the patency status of the IRA. CONCLUSIONS: ST segment elevation in leads V7 to V9 identifies patients with a larger inferior MI because of concomitant posterolateral involvement. Such patients might benefit more from thrombolytic therapy.

Effect of thrombolytic therapy on the evolution of significant mitral regurgitation in patients with a first inferior myocardial infarction.

OBJECTIVES: This study was designed to test the hypothesis that reperfusion therapy with thrombolysis will prevent the development of significant mitral regurgitation in patients with inferior myocardial infarction. BACKGROUND: The value of thrombolytic therapy in patients with inferior or posterior wall myocardial infarction has been controversial. We hypothesized that successful reperfusion therapy with intravenous thrombolysis may reduce the incidence and severity of postinfarction mitral regurgitation in this patient group. METHODS: We prospectively studied 104 patients with a first inferior myocardial infarction. Thrombolytic therapy was administered to 55 patients (treatment group) 3.2 +/- 2.1 h after the onset of symptoms. The other 49 patients formed the control group. Doppler echocardiographic color flow imaging was performed in all patients within 24 h, at 7 to 10 days and at 28 to 30 days after myocardial infarction. Significant mitral regurgitation was defined as moderate or severe (grade 2 or 3). RESULTS: No significant differences in baseline clinical characteristics were observed between the treatment and control groups. The overall incidence rates of significant mitral regurgitation at 24 h, 7 to 10 days and at 28 to 30 days were 10 (10%) of 104 patients, 18 (17%) of 104 patients and 11 (11%) of 100 patients, respectively. Multivariate analysis reveals the following independent predictors of the occurrence of significant mitral regurgitation: female gender (at 7 to 10 days, odds ratio 5.3, 90% confidence interval [CI] 1.8 to 15.5; at 28 to 30 days, odds ratio 3.7, 90% CI 1.1 to 12.7), heart failure (at 7 to 10 days, odds ratio 7.7, 90% CI 2.2 to 26.9) and transient complete atrioventricular block (at 24 h of myocardial infarction, odds ratio 5.8, 90% CI 1.2 to 27). Compared with the control group, the treatment group exhibited marked reduction in the incidence of significant mitral regurgitation at 24 h (16% vs. 4%; odds ratio 0.1, 90% CI 0.0 to 0.7); at 7 to 10 days (24% vs. 11%; odds ratio 0.3, 90% CI 0.1 to 0.9) and at 28 to 30 days (15% vs. 7%; odds ratio 0.4, 90% CI 0.1 to 1.6). Severe (grade 3) mitral regurgitation developed in five patients in the control group but in no patient in the treatment group. CONCLUSIONS: Thrombolytic therapy in the patients with a first inferior myocardial infarction was associated with a reduced incidence of significant mitral regurgitation. These results support the use of such therapy in patients with inferior myocardial infarction.

Left ventricular pseudohypertrophy in cardiac tamponade: an echocardiographic study in a canine model.

OBJECTIVES: This study was designed to establish whether left ventricular pseudohypertrophy in cardiac tamponade can be reproducibly induced in an experimental canine model and to investigate the mechanism of its production. BACKGROUND: Past experimental and clinical studies have shown reduction of ventricular volumes resulting from cardiac tamponade. Left ventricular pseudohypertrophy, a transient thickening of myocardial walls, was recently described as a new echocardiographic sign of cardiac tamponade. METHODS: Cardiac tamponade was induced in seven anesthetized open chest dogs with serial bolus injections of 50 ml each of 0.9% saline solution into the pericardial sac. Under hemodynamic monitoring, M-mode and two-dimensional echocardiographic measurements were performed from a right parasternal window at each stage of graded cardiac tamponade. RESULTS: There was a progressive increase of interventricular septal and posterior wall diastolic thickness. Mean wall thickness (interventricular septal thickness + posterior wall thickness divided by 2) was 9.8 +/- 1.3 mm at baseline, 14.3 +/- 0.9 mm at peak tamponade and 9.0 +/- 1.5 mm after fluid withdrawal (p < 0.0001). Mean wall thickness correlated directly with the severity of cardiac tamponade, as estimated from the level of right arterial pressures (r = 0.75 and p < 0.0001), and with the decrease of left ventricular cavity volume (r = -0.67 and p < 0.0001). Left ventricular mass did not change significantly. CONCLUSIONS: Left ventricular pseudohypertrophy is a constant manifestation of cardiac tamponade in a canine model. The degree of myocardial thickening correlates with the reduction of ventricular dimensions and with the severity of hemodynamic compromise, representing a constant facet of heart remodeling in cardiac tamponade.

The distinction between coronary and myocardial reperfusion after thrombolytic therapy by clinical markers of reperfusion.

OBJECTIVES: We sought to examine the hypothesis that rapid resolution of ST-segment elevation in acute myocardial infarction (AMI) patients with early peak creatine kinase (CK) after thrombolytic therapy differentiates among patients with early recanalization between those with and those without adequate tissue (myocardial) reperfusion. BACKGROUND: Early recanalization of the epicardial infarct-related artery (IRA) during AMI does not ensure adequate reperfusion on the myocardial level. While early peak CK after thrombolysis results from early and abrupt restoration of the coronary flow to the infarcted area, rapid ST-segment resolution, which is another clinical marker of successful reperfusion, reflects changes of the myocardial tissue itself. METHODS: We compared the clinical and the angiographic results of 162 AMI patients with early peak CK (< or =12 h) after thrombolytic therapy with (group A) and without (group B) concomitant rapid resolution of ST-segment elevation. RESULTS: Patients in groups A and B had similar patency rates of the IRA on angiography (anterior infarction: 93% vs. 93%; inferior infarction: 89% vs. 77%). Nevertheless, group A versus B patients had lower peak CK (anterior infarction: 1,083+/-585 IU/ml vs. 1,950+/-1,216, p < 0.01; and inferior infarction: 940+/-750 IU/ml vs. 1,350+/-820, p=0.18) and better left ventricular ejection fraction (anterior infarction: 49+/-8, vs. 44+/-8, p < 0.01; inferior infarction: 56+/-12 vs. 51+/-10, p=0.1). In a 2-year follow-up, group A as compared with group B patients had a lower rate of congestive heart failure (1% vs. 13%, p < 0.01) and mortality (2% vs. 13%, p < 0.01). CONCLUSIONS: Among patients in whom reperfusion appears to have taken place using an early peak CK as a marker, the coexistence of rapid resolution of ST-segment elevation further differentiates among patients with an opened culprit artery between the ones with and without adequate myocardial reperfusion.

Underestimation of extent and severity of coronary artery disease by dipyridamole stress thallium-201 single-photon emission computed tomographic myocardial perfusion imaging in patients taking antianginal drugs.

OBJECTIVES: This study evaluated the diagnostic value of dipyridamole plus low level treadmill exercise (dipyridamole stress) thallium-201 single-photon emission computed tomography (SPECT) in patients taking antianginal drugs. BACKGROUND: Dipyridamole stress is the major substitute for maximal exercise in patients referred for myocardial perfusion imaging. Although antianginal drugs are commonly suspended before exercise, dipyridamole stress is usually performed without discontinuing these drugs. METHODS: Twenty-six patients underwent two dipyridamole perfusion studies: the first without (SPECT-1) and the second with (SPECT-2) antianginal treatment. Twenty-one patients (81%) received calcium antagonists, 19 (73%) received nitrates, and 8 (31%) received beta-blockers. Eighteen of the patients underwent coronary angiography. Data are presented as the mean value +/- SD. RESULTS: Visual scoring yielded significantly larger and more severe reversible perfusion defects for SPECT-1 than for SPECT-2. Quantitative analysis showed larger perfusion defects on stress images of SPECT-1 in the left anterior descending coronary artery (LAD) (25 +/- 21% vs. 17 +/- 15%, p = 0.003), left circumflex coronary artery (LCx) (56 +/- 35% vs. 48 +/- 36%, p = 0.03) and right coronary artery (RCA) (36 +/- 27% vs. 25 +/- 24%, p = 0.008) territories. Individual vessel sensitivities in the LAD, LCx and RCA territories were 93%, 79% and 100% for SPECT-1 and 64%, 50% and 70% for SPECT-2, respectively. These differences were highly significant for the LAD (p = 0.004) and LCx (p = 0.00004) territories. The overall individual vessel sensitivity of SPECT-1 was significantly higher than that of SPECT-2 (92% vs. 62%, p = 0.000003). Specificity was not significantly different in SPECT-1 compared with SPECT-2 (80% and 93%, p = 0.33). CONCLUSIONS: Continued use of antianginal drugs before dipyridamole plus low level treadmill exercise thallium-201 SPECT may reduce the extent and severity of myocardial perfusion defects, resulting in underestimation of coronary artery disease.

Should thrombolytic therapy be administered in the mobile intensive care unit in patients with evolving myocardial infarction? A pilot study.

The growing recognition of the importance of early thrombolysis in evolving myocardial infarction was the basis for the present study, which evaluated the effectiveness, feasibility and safety of prehospital thrombolytic therapy. In a relatively small study, 118 patients were allocated to receive either prehospital treatment with recombinant tissue-type plasminogen activator (rt-PA) in the mobile intensive care unit (group A, 74 patients) or hospital treatment (group B, 44 patients). A total of 120 mg of rt-PA was infused over a period of 6 h. All patients were fully heparinized and underwent radionuclide left ventriculography and coronary angiography during hospitalization. Although group A was treated significantly earlier than group B after onset of symptoms (94 +/- 36 versus 137 +/- 45 min, respectively; p less than 0.001), no significant differences were observed between the groups in 1) extent of myocardial necrosis, 2) global left ventricular ejection fraction at discharge, 3) patency of infarct-related artery, 4) length of hospital stay, and 5) mortality at 60 days. However, a trend to a lower incidence of congestive heart failure at hospital discharge was observed in the prehospital-treated compared with the hospital-treated group (7% versus 16%, respectively; p = NS). No major complications occurred during transportation. It is concluded that myocardial infarction can be accurately diagnosed and thrombolytic therapy initiated relatively safely during the prehospital phase by the mobile intensive care team, thus instituting a beneficial clinical trend in favor of prehospital thrombolysis.

Q wave and Non-Q wave myocardial infarction after thrombolysis.

OBJECTIVES: We studied the clinical outcome of Q wave and non-Q wave infarction after thrombolytic therapy. BACKGROUND: Controversy exists over the clinical significance of Q waves after thrombolysis. METHODS: We studied postthrombolytic angiographic results and short- and long-term clinical outcome in 150 patients with acute myocardial infarction classified as Q wave and non-Q wave on the 24-h and discharge electrocardiograms (ECGs). The results from the two groups were then compared. RESULTS: Eighty percent of patients had a Q wave and 20% a non-Q wave infarction on the 24-h ECG. The latter patients had lower peak creatine kinase (CK) levels (p < 0.001), but the two groups did not differ significantly otherwise. In 18 patients with a Q wave infarction on the 24-h ECG, pathologic Q waves disappeared. However, in seven patients with a non-Q wave infarction on the 24-h ECG, pathologic Q waves appeared throughout the hospital period. Q wave regression was associated with lower peak CK levels (p < 0.001) and an improvement in left ventricular ejection fraction (p < 0.01). Thus, only 72% of patients had a Q wave and 28% a non-Q wave infarction on the discharge ECG. Patients with a non-Q wave infarction on the discharge ECG had higher patency of the infarct-related artery (p < 0.04), lower mean peak CK levels (p < 0.0001), a higher ejection fraction (p = 0.001) and a lower incidence of heart failure (p = 0.06) than patients with a Q wave infarction on the discharge ECG. Although the 2-year incidence of reinfarction and revascularization was higher in patients with a non-Q wave infarction on the discharge ECG (p < 0.05), 2-year mortality was lower (p = 0.08). CONCLUSIONS: Although the early postthrombolytic distinction between Q wave and non-Q wave infarction conveys no significant information, during the hospital period, non-Q wave infarction is associated with a smaller infarct area, improved left ventricular function and lower mortality.

Early T wave inversion after thrombolytic therapy predicts better coronary perfusion: clinical and angiographic study.

OBJECTIVES: This study was undertaken to test the hypothesis that early inversion of T waves after thrombolytic therapy for acute myocardial infarction predicts patency of the infarct-related artery with high Thrombolysis in Myocardial Infarction (TIMI) perfusion flow and better in-hospital outcome. BACKGROUND: Although numerous studies have demonstrated a strong association between early resolution of ST segment elevation after acute myocardial infarction and successful thrombolysis, little is known about early changes in T waves after thrombolytic therapy. METHODS: Ninety-four consecutive patients with acute myocardial infarction treated with recombinant tissue-type plasminogen activator (rt-PA) were studied with admission and predischarge radionuclide ventriculography and with coronary angiography within 72 h of admission. Patient stratification was based on the presence or absence of early (within 24 h) T wave inversion. RESULTS: Early T wave inversion was associated with a higher patency rate of the infarct-related artery (90% vs. 65%, p < 0.02) and less severe residual stenosis ([mean +/- SD] 73 +/- 27 vs. 83 +/- 22, p = 0.06), and when only TIMI perfusion grade 3 was considered, the difference was even greater (77% vs. 41%, p < 0.001). Patients with early inversion of T waves had a lower peak creatine kinase value ([mean +/- SD] 678 +/- 480 vs. 1,076 +/- 620, p < 0.01), and although a similar percent of patients with and without early T wave inversion had a normal ejection fraction (> or = 55%) on admission, a higher percent of patients with early inversion had a normal ejection fraction at hospital discharge (71% vs. 44%, p < 0.03). Early T wave inversion anticipated a more benign in-hospital clinical course with a lower incidence of adverse cardiac events (10% vs. 33%, p < 0.02). CONCLUSIONS: Early inversion of T waves in patients with acute myocardial infarction treated with thrombolytic therapy suggests patency of the infarct-related artery, better perfusion grade and left ventricular function and a more benign in-hospital course.

The significance of persistent ST elevation versus early resolution of ST segment elevation after primary PTCA.

OBJECTIVES: To determine the prevalence and clinical significance of early ST segment elevation resolution after primary percutaneous transluminal coronary angioplasty (PTCA) for acute myocardial infarction (AMI). BACKGROUND: Despite angiographically successful restoration of coronary flow early during AMI, adequate myocardial reperfusion might not occur in a substantial portion of the jeopardized myocardium due to microvascular damage. This phenomenon comprises the potentially beneficial effect of early recanalization of the infarct related artery (IRA). METHODS: Included in the study were 117 consecutive patients who underwent angiographically successful [Thrombolysis in Myocardial Infarction (TIMI III)] primary PTCA. The patients were classified based on the presence or absence of reduction > or =50% in ST segment elevation in an ECG performed immediately upon return to the intensive cardiac care unit after the PTCA in comparison with ECG before the intervention. RESULTS: Eighty-nine patients (76%) had early ST segment elevation resolution (Group A) and 28 patients (24%) did not (Group B). Group A and B had similar clinical and hemodynamic features before referring to primary PTCA, as well as similar angiographic results. Despite this, ST segment elevation resolution was associated with better predischarge left ventricular ejection fraction (LVEF) (44.7 +/- 8.0 vs. 38.2 +/- 8.5, p < 0.01). Group B patients, as compared with those of Group A, had a higher incidence of in-hospital mortality (11% vs. 2%, p = 0.088), congestive heart failure (CHF) [28% vs. 19%, odds ratio (OR) = 4, 95% confidence interval (CI) 1 to 15, p = 0.04], higher long-term mortality (OR = 7.3, 95% CI 1.9 to 28, p = 0.004 with Cox proportional hazard regression analysis) and long-term CHF rate (OR = 6.5, 95% CI 1.3 to 33, p = 0.016 with logistic regression). CONCLUSIONS: Absence of early ST segment elevation resolution after angiographically successful primary PTCA identifies patients who are less likely to benefit from the early restoration of flow in the IRA, probably because of microvascular damage and subsequently less myocardial salvage.