History Of Remote Myocardial Infarction Research Articles

Biomarkers of inflammation and fibrosis in young adults with history of Kawasaki disease.

BackgroundMyocardial histology from autopsies of young adults with giant coronary artery aneurysms following Kawasaki disease (KD) shows bridging fibrosis beyond the territories supplied by the aneurysmal arteries. The etiology of this fibrosis is unknown, but persistent, low-level myocardial inflammation and microcirculatory ischemia are both possible contributing factors. To investigate the possibility of subclinical myocardial inflammation or fibrosis, we measured validated biomarkers in young adults with a remote history of KD.MethodsWe measured plasma calprotectin, galectin-3 (Gal-3), growth differentiation factor-15 (GDF-15), soluble ST2 (sST2), and serum procollagen type 1C-terminal propeptide (P1CP) in 91 otherwise healthy young adults with a remote history of KD and in 88 age-similar, healthy controls. KD subjects were stratified by coronary artery aneurysm (CAA) status and history of remote myocardial infarction (MI).ResultsAfter correction for multiple testing, calprotectin, Gal-3, and GDF-15 levels were significantly higher in subjects with persistent CAA (n = 26) compared with KD subjects with remodeled CAA (n = 20, p = 0.005, 0.001, 0.0036, respectively). In a multivariable regression model with CA status as the main predictor and adjusting for sex, MI history, and interval from KD onset, CA status was a significant predictor (Persistent CAA vs KD Normal CA) of calprotectin, Gal-3, GDF-15 and sST2 levels (p = 0.004, <0.001, 0.007, and 0.049, respectively).ConclusionsThese results suggest that ongoing inflammation and fibrosis may be occurring in individuals with persistent CAA. Longitudinal follow-up is needed to clarify the clinical significance of these elevated biomarker levels in this patient population that requires life-long monitoring.

Diagnosis of Type III Endoleak and Endovascular Treatment with Aortouniiliac Stent-Graft

The present report describes a case of type III endoleak from a tear in the fabric of a Zenith bifurcated stent-graft approximately 6 months after implantation. The reason of the fabric tear was unknown. The complication was successfully treated by aortouniiliac stent-graft implantation followed by creation of a femorofemoral bypass.

Wide-complex tachycardias. The importance of identifying the mechanism.

Initial assessment of widecomplex tachycardias (WCTs) should begin with patient history and physical examination. If there is a history of remote myocardial infarction, WCT should be considered as ventricular tachycardia until proved otherwise. In most cases, WCT is subsequently shown by electrophysiologic evaluation to be ventricular tachycardia. The presenting symptoms and degree of hemodynamic compromise should not be used to distinguish ventricular tachycardia from supraventricular tachycardia. A 12-lead electrocardiogram (ECG) should be carefully reviewed by looking for signs of ventricular tachycardia (atrioventricular dissociation, captured and fusion beats, certain QRS shapes and concordance). If the surface ECG is inconclusive, changing the position of V1 or use of a transesophageal lead may allow assessment of atrial activity. When more QRS than P waves are documented, the diagnosis is ventricular tachycardia. Cardioversion-defibrillation is required in patients with WCT who are in unstable condition. Atrioventricular node blockers are the agents of choice for arrhythmias that are atrioventricular node-dependent, but they may cause hemodynamic collapse if administered to patients with ventricular tachycardia or with atrial fibrillation and preexcitation. Lidocaine hydrochloride (Xylocaine HCl IV), preferred for ventricular tachycardia, has been reported to cause ventricular fibrillation in patients with atrial fibrillation and preexcitation. When there is doubt about the diagnosis, elective electrical cardioversion may be considered. Medical therapy should consist of intravenous magnesium sulfate and procainamide hydrochloride (Pronestyl). A beta blocker may also be considered if more aggressive blockade of the atrioventricular node becomes necessary.

Concealed entrainment as a guide for catheter ablation of ventricular tachycardia in patients with prior myocardial infarction

Fifteen consecutive patients with drug-refractory, recurrent, sustained, monomorphic ventricular tachycardia and a history of remote myocardial infarction underwent catheter ablation of ventricular tachycardia. Shocks of 100 to 300 J were delivered to sites at which pacing during ventricular tachycardia resulted in concealed entrainment, in which the ventricular tachycardia accelerated to the pacing rate, there was a long stimulus to QRS interval and there was no change in the configuration of the QRS complex during pacing at several rates compared with the configuration during ventricular tachycardia, thus identifying a zone of slow conduction in the reentrant circuit. Concealed entrainment was demonstrated in nine (60%) of 15 patients, and the stimulus to QRS intervals were 90 to 400 ms. At sites of concealed entrainment, the endocardial activation time relative to the QRS complex during ventricular tachycardia ranged from -125 to +50 ms, the timing of the local electrogram relative to the QRS complex was the same during entrainment as during ventricular tachycardia and the pace map during sinus rhythm was discordant with that of the ventricular tachycardia in seven patients. In the six patients in whom a site of concealed entrainment could not be identified, the target site for ablation was selected on the basis of identification of an isolated mid-diastolic potential, activation mapping and pace mapping. The mean (+/- SD) cumulative number of joules delivered to the target site was 306 +/- 140. A successful long-term clinical outcome was achieved in 9 of the 15 patients (mean follow-up 20 +/- 7 months). The clinical success rate was the same whether the target site was selected on the basis of concealed entrainment (five of nine, 56%) or on the basis of the other mapping techniques (four of six, 67%). In conclusion, the responses to pacing suggest that sites at which there is concealed entrainment may be located within a zone of slow conduction in the ventricular tachycardia reentry circuit, although not necessarily in an area critical for the maintenance of reentry. The long-term clinical efficacy of catheter ablation targeted to sites of concealed entrainment is about 60%, similar to the results achieved when conventional mapping techniques are used.

Wide QRS Tachycardia in the Conscious Adult

Hemodynamic stability during wide QRS tachycardia is commonly, albeit erroneously, taken as evidence for a supraventricular mechanism. To determine the magnitude for potential misdiagnosis in applying this notion clinically, we analyzed 20 consecutive cases of regular wide QRS tachycardia in conscious adult patients (mean age, 64 years). The most common heart disease was atherosclerotic (75%), with an associated history of remote myocardial infarction in 73% of the cases. Tachycardia was sustained for a mean of 4.8 hours prior to medical evaluation, with a mean rate of 186 beats per minute and mean systolic blood pressure of 111 mm Hg. A diagnosis of ventricular tachycardia (VT) was established in 17 cases (85%). In the patients with VT, atrioventricular dissociation was recognized on the 12-lead electrocardiogram in 38%, with Wellens' morphological features favoring the diagnosis in 73%. Following conversion to sinus rhythm, electrophysiological testing in 17 patients reproduced the clinical arrhythmia in 94% (with a replication rate of 100% in 15 patients with VT), with at least one additional unsuspected VT morphology induced in 53% of patients with VT. Thus, VT should be considered the most likely cause of regular wide QRS tachycardia in the conscious adult patient, especially with a history of remote myocardial infarction. Recognition of this simple principle and careful examination of the 12-lead electrocardiogram may help to prevent the misapplication of pharmacotherapy in the vast majority of these patients.

Delineation of impaired regional myocardial perfusion by positron emission tomography with H2(15)O.

Positron emission tomography with 15O-labeled water (H2(15)O) can be used to delineate abnormal regional myocardial blood flow in experimental animals. To determine the feasibility of this method in humans, we studied 33 subjects (9 normal volunteers and 24 patients with angiographically documented coronary artery disease) at rest and after myocardial hyperemia induced with intravenous infusion of dipyridamole. At rest, the myocardial region demonstrating the lowest relative H2(15)O activity exhibited 71 +/- 8% of activity in the region with peak activity in control subjects and 62 +/- 17% in patients (p = NS). After the dipyridamole infusion, differences between the two groups were accentuated. In control subjects, activity in the region with lowest relative radioactivity averaged 77 +/- 5% of that in the region with peak activity. In patients, it averaged 55 +/- 22% of activity in the region with peak activity (p less than 0.01). Results in patients with ischemia with or without a history of remote myocardial infarction were not significantly different. In 22 of the 24 patients, the region with lowest relative perfusion corresponded anatomically to the region of myocardium distal to a stenosis. Thus, delineation of regional myocardial perfusion in patients with coronary artery disease is possible with positron emission tomography and H2(15)O. Further studies will be necessary to prospectively determine sensitivity and specificity.

Flecainide: Steady state electrophysiologic effects in patients with remote myocardial infarction and inducible sustained ventricular arrhythmia

The effect of flecainide in 24 patients with inducible sustained ventricular arrhythmia and a history of remote myocardial infarction was determined. Flecainide was administered in oral doses individually adjusted to suppress all spontaneous ventricular tachycardia and 80% of ventricular premature complexes on 24 hour ambulatory (Holter) electrocardiography. Antiarrhythmic therapy, as assessed by Holter monitoring, was adequate in 20 (83%) of the study patients at a mean dose of 144 +/- 28 mg every 12 hours; the mean plasma flecainide level was 583 +/- 329 ng/ml. In 18 patients, the mean sinus cycle length, sinus node recovery time and atrial, atrioventricular nodal and ventricular refractory periods were unchanged. The AH interval increased by 15 +/- 15%, the HV interval by 35 +/- 32% and the QRS duration by 24 +/- 21%. Toxicity or failure to suppress ventricular premature complexes and ventricular tachycardia by Holter monitoring precluded electrophysiologic study with flecainide in four patients; two patients refused electrophysiologic study with flecainide for nonmedical reasons. Ventricular tachycardia was not inducible in 4 (22%) of 18 patients receiving flecainide. Sustained arrhythmia remained inducible in 14 patients (78%) despite evidence of antiarrhythmic efficacy on Holter monitoring, but the rate of the induced ventricular tachycardia was slower and symptoms were alleviated during ventricular tachycardia in 10 (56%) of 18 patients. The 4 patients who had no inducible ventricular tachycardia with flecainide, and the 10 patients who had inducible ventricular tachycardia with a longer cycle length and alleviation of their symptoms, have been followed up as outpatients for 16 +/- 7 months.(ABSTRACT TRUNCATED AT 250 WORDS)

Aorto-coronary bypass surgery in 62 patients with severe left ventricular dysfunction--a follow-up study.

Long-term follow-up of 62 consecutive patients with severe left ventricular dysfunction (ejection fraction = less than 0.30) and disabling angina pectoris following aorto-coronary bypass surgery was investigated. Prior to surgery all patients had angina pectoris and a history of remote myocardial infarction, 35% were in congestive heart failure (CHF). Significant stenoses in 3 major coronary vessels were present in 51 patients (82%). An average of 3.5 grafts per patient were employed. Operative mortality (30 days) rate was 4.8% (3 patients) and 13 patients died during the following period. The average follow-up was 37 months (range: 6 to 116 months). At follow-up, the 5-year survival probability for these patients was 70% (SD = 9%). Thirty-one patients (67%) of the 46 survivors had complete relief of angina, but signs of CHF were still evident in 17 patients (36%). Compared to patients with ejection fractions above 0.30% (surgical mortality 1.4% and 5-year survival rate 94% (SD = 3%] the outcome of coronary artery bypass grafting in patients with poor left ventricular function showed a significantly higher surgical mortality (P = 0.03) and impaired long-term survival (P = 0.02). However, aorto-coronary bypass grafting can be performed in patients with severe left ventricular dysfunction with reasonable relief of angina and with an acceptable surgical mortality.

Association between leukocyte count and the presence and extent of coronary atherosclerosis as determined by coronary arteriography

Angiographic evidence of coronary artery disease (CAD) was correlated with leukocyte count (WBC), red cell count (RBC), cigarette smoking, age, sex, and cholesterol and triglyceride concentrations in 573 patients who underwent coronary arteriography and who did not have evidence of infection or recent myocardial infarction. Smokers had a higher WBC (7,449 ± 1,964leukocytes/mm 3 vs 6,533 ± 1,557, p = 0.0001) and RBC (4.921 × 10 6 ± 0.491 × 10 6 erythrocytes/mm 3 vs 4.753 × 10 6 ± 0.480 × 10 6 p = 0.0001) than nonsmokers. Patients with CAD had a higher WBC (7,280 ± 1,926 vs 6,664 ± 1,700, p = 0.0005) and RBC (4.903 × 10 6 ± 0.488 vs 4.777 × 10 6 ± 0.485 × 10 6, p = 0.0062) than those with normal coronary arteriograms. A positive correlation between WBC and the severity of CAD (sum of arterial diameter narrowing) was noted (r = 0.16, p = 0.0001). Multiple regression showed an independent contribution of WBC in predicting severity of CAD (F = 9.26, p = 0.0025), after accounting for the effects of age, sex, serum cholesterol and triglyceride levels. When smoking was entered into the equation, the contribution of WBC in predicting the severity of angiographic CAD became weaker (F = 4.46, p = 0.035). Similar relations were seen when only smokers were analyzed and when patients with history of remote myocardial infarction were excluded. In nonsmokers these associations became either insignificant or much weaker. Thus, the relation of WBC, and RBC with CAD is mainly due to the elevation of WBC and RBC and the increase of CAD risk induced by cigarette smoking.

Diagnosis and treatment of a case of recurrent ventricular tachycardia

A man with a history of remote myocardial infarction developed refractory recurrent tachyarrhythmia with widened QRS complexes. Conversion to sinus rhythm during administration of intravenous vasopressors occurred on several occasions, and the arrhythmia was considered to be supraventricular tachycardia with aberration of the QRS. Atrial recording, competitive atrial pacing, and Holter monitoring were used to establish a diagnosis of ventricular tachycardia. Subsequent to coronary artery bypass surgery and partial excision of a noncontractile scar from the posterior wall of the left ventricle, he has had no further tachyarrhythmias. The difficulties in differential diagnosis and the techniques used are discussed.