Prevalence of abdominal aortic aneurysm in patients referred for transthoracic echocardiography.

BACKGROUND: Previous studies have documented the prevalence of abdominal aortic aneurysm (AAA) during transthoracic echocardiography, but the effect of such screening on subsequent vascular interventions remains unclear. AIM: This study aimed to determine the utility of opportunistic selective screening for AAA in a contemporary large series of patients having transthoracic echocardiography. METHODS: Subjects aged 50 years or older having transthoracic echocardiography had scanning of the infrarenal aorta in a consecutive series of 10 403 men and women. RESULTS: The study subjects had a mean age of 70.2 ± 10.7 years, and 54.1% were men. There was a 3.5% (95% confidence interval (CI) 3.2-3.9%) prevalence of AAA with a median diameter of 39 mm (interquartile range 32 mm-48 mm). In males ≥ 65 years the prevalence of newly diagnosed AAA was 6.2% (95% CI 5.5-7.0%). Of those with newly diagnosed AAA, 39.7% underwent AAA repair. Age and male gender were associated with AAA prevalence. After adjustment for age and gender, echocardiographic variables associated with AAA were left ventricular end diastolic dimension (odds ratio (OR) 1.02, 95%CI 1.01-1.04), interventricular septum thickness (OR 1.11, 95% CI 1.06-1.17), left ventricular posterior wall thickness (OR 1.09, 95% CI 1.03-1.15), left atrial diameter (OR 1.04, 95% CI 1.02-1.07) and aortic root diameter (OR 1.09, 95% CI 1.06-1.11). CONCLUSIONS: This study revealed a high prevalence of newly diagnosed AAA in a group of older men having cardiac evaluation. There was a relationship of increasing age with AAA, and a significant proportion of newly diagnosed subjects were not suitable for AAA repair.

Clinical recognition of neurally mediated syncope.

BACKGROUND: Most cases of syncope are due to hypotension, with a vasovagal response the commonest single mechanism. Neurally mediated syncope (NMS) is a vasovagal response evoked by common physical or psychological stress factors in susceptible individuals. Although upright tilt table testing (TTT) has been developed to diagnose this condition, the clinical recognition of this common syndrome in the general community remains poor. AIMS: To evaluate the clinical presentation of patients with NMS and pre-syncope, proven by TTT, and compare them to patients with syncope that have a low probability of having NMS (e.g. older patients with cardiac disease and negative TTT). METHODS: Prospective evaluation by questionnaire at the time of TTT, including documentation of presenting symptoms and signs, and provoking factors in consecutive patients. Comparisons between patient groups analyzed using chi-squared tests and logistic regression. RESULTS: Neurally mediated syncope patients were more likely to present with both syncope and pre-syncope, often with prolonged histories of pre-syncope. Certain provoking stress factors were more common in NMS, with multiple factors often present. Most NMS patients had a hypotensive prodrome before syncope, whereas control patients had a higher incidence of syncope without warning. CONCLUSION: Neurally mediated syncope patients present with situational syncope that is not only stereotypical for the individual, but shares common features with other similar patients. While none of the clinical observations is unique to NMS, a carefully detailed history can elicit a convincing diagnostic pattern that can often obviate the need for extensive and expensive investigation, and in younger patients a TTT may not be required to make the diagnosis.

Lack of association between baseline plasma homocysteine concentrations and restenosis rates after a first elective percutaneous coronary intervention without stenting.

OBJECTIVE: To evaluate the association between baseline homocysteine concentrations and restenosis rates in patients electively undergoing their first percutaneous coronary intervention (PCI) without stenting. DESIGN: Prospective, single centre, observational study. SETTING AND PATIENTS: Patients electively undergoing their first PCI without stenting at a tertiary referral centre between 1990 and 1998. METHODS: Blood samples were collected from all patients at baseline and assayed to determine the patients' homocysteine concentrations. Patients whose PCI was successful underwent repeat angiography at a median of 6.4 (interquartile range 6-6.8) months. Their baseline and follow up angiograms were compared by quantitative coronary angiography to assess the incidence of restenosis. For the analysis, the patients were divided into two groups based on whether their baseline homocysteine concentrations were above or below the median value. These two groups were compared to determine whether there was any association between their baseline homocysteine concentrations and the incidence of restenosis at six months. RESULTS: 134 patients had a successful first PCI without stenting (involving 200 lesions). At six month angiography, restenosis was observed in 33 patients (49.3%) with baseline homocysteine concentrations above the median value and in 31 patients (46.3%) with concentrations below the median value (p = 0.74). There was no difference in the percentage of lesions developing restenosis (38 (39.6%) v 40 (38.5%), respectively, p = 0.87) or late lumen loss (0.40 mm v 0.31 mm, respectively, p = 0.24). On multivariable analysis, there was no association between homocysteine concentrations and late lumen loss (r = -0.11, p = 0.11) or the percentage diameter stenosis at follow up (r = -0.07, p = 0.32). CONCLUSION: Baseline homocysteine concentrations were not associated with six month restenosis rates in patients electively undergoing their first PCI without stenting.

Relation of heart rate variability and serum lipoproteins in type 1 diabetes mellitus and chronic stable angina pectoris.

This investigation examines whether serum lipoprotein levels in patients with diabetes mellitus and in those with coronary artery disease are associated with lower heart rate variability (HRV). The study group consisted of 58 subjects divided into 3 groups: normal subjects, chronic stable angina, and type 1 diabetes. Twenty-four-hour ambulatory electrocardiographic recordings were analyzed in the time and frequency domains; standard instantaneous autonomic testing was also performed. On 24-hour ambulatory recordings, patients with chronic stable angina had significantly lower HRV than normals, and diabetics had a more marked reduction in HRV than both normals and anginal patients. When anginal patients and diabetics were stratified by total serum and low-density lipoprotein (LDL) cholesterol levels, diabetics with elevated total and LDL cholesterol had an additional, significant decrease in HRV parameters. No such difference was demonstrated in patients with stable angina. No significant correlations were noted for high-density lipoprotein (HDL) cholesterol, triglycerides, or total cholesterol/HDL ratio and HRV in diabetics or patient with angina. Diabetics with markedly abnormal peripheral reflexes had significantly higher triglycerides and total cholesterol/HDL ratios. Finally, standard tests of autonomic function did not correlate with total, LDL, HDL cholesterol levels, total cholesterol/HDL ratio, or triglycerides. Thus, we found a relation between atherogenic lipid levels and reduced HRV in diabetic patients that has not been previously identified.

Frequent reocclusion of patent infarct-related arteries between 4 weeks and 1 year: effects of antiplatelet therapy.

OBJECTIVES: This study assessed the effect of the combination of aspirin and dipyridamole on patency of the infarct-related artery between 4 weeks and 1 year after myocardial infarction. BACKGROUND: Patency of the infarct-related artery is an important determinant of prognosis after myocardial infarction. The incidence of late reocclusion and the effects of antiplatelet therapy are unknown. METHODS: To investigate the importance of antiplatelet therapy for the prevention of late reocclusion, 215 patients who had a patent infarct-related artery 4 weeks after myocardial infarction were randomized in a double-blind manner to receive either a combination of 25 mg of aspirin and 200 mg of dipyridamole twice daily or placebo. One hundred fifty-four patients underwent further coronary arteriography 1 year later. RESULTS: At 1 year, 38 (25%) of 154 patients had reocclusion of the infarct-related artery; 18 (23%) of 79 patients receiving aspirin and dipyridamole had late reocclusion versus 20 (27%) of 75 who received placebo (p = NS). The rate of reocclusion was related to the severity of the residual coronary artery stenosis at 4 weeks (< 50% stenosis 9.2%; 50% to 69% stenosis 11.6%; 70% to 89% stenosis 30.4%; > or = 90% stenosis 70%, p < 0.01). The majority of reocclusions were silent, and only 17 (45%) of 38 were clinically associated with further infarction. There were no differences for a hierarchic end point of cardiac death, myocardial infarction or revascularization (14.8% aspirin and dipyridamole vs. 17.8% placebo). CONCLUSIONS: Late reocclusion of the patent infarct-related artery is a frequent event, occurring in 25% of patients. Antiplatelet therapy with the combination of aspirin and dipyridamole does not alter the overall rate of late reocclusion. Other strategies are required to reduce late reocclusion.

End-systolic volume and long-term survival after coronary artery bypass graft surgery in patients with impaired left ventricular function.

BACKGROUND: Left ventricular function is the main predictor of long-term survival in patients with coronary artery disease. In patients with impaired left ventricular function after myocardial infarction, end-systolic volume is a better predictor than the global ejection fraction. We analyzed long-term follow-up of patients with impaired left ventricular function undergoing coronary artery bypass graft surgery to evaluate preoperative predictors of survival. METHODS AND RESULTS: Consecutive patients with ejection fractions < or = 40% (n = 193) who had undergone surgical revascularization were followed to assess the predictive value of preoperative baseline characteristics and catheterization findings for long-term survival. Patients were followed for 133 +/- 30.7 months. At the time of surgery, patient age was 56 +/- 7.9 years and 169 patients (87.6%) had a history of previous myocardial infarction. Thirty-one patients (16%) were female. The ejection fraction was 32 +/- 7%, and the end-systolic volume was 147.4 +/- 52.6 mL. One hundred sixty-four patients (84.9%) had three-vessel disease, and 44 (22.8%) had a left main stenosis with > 50% diameter loss. Follow-up was complete in 99%. Fourteen patients died (7.3%) within the first 30 days after surgery. Twelve-month actuarial survival was 86%, 4-year survival was 80%, and 10-year survival was 40%. Predictors of poor long-term survival on multivariate analysis were end-systolic volume index (chi 2 = 14.02, P = .002), number of previous myocardial infarctions (chi 2 = 6.47, P = .001), preoperative stenosis score (chi 2 = 4.97, P = .02), and age at the time of surgery (chi 2 = 4.45, P = .03). CONCLUSIONS: End-systolic volume index is the major predictor of survival after coronary artery bypass graft surgery in patients with impaired left ventricular function. Strategies to prevent ventricular dilatation, such as angiotensin-converting enzyme inhibitors, may improve the long-term outcome in these patients.

Diagnosis of left atrial myxoma at routine coronary angiography in an asymptomatic patient.

Asymptomatic atrial myxomas are very rare and are usually diagnosed at echocardiography. Abnormal left atrial vascularity was seen as an incidental finding in an asymptomatic patient at coronary angiography. Transesophageal echocardiography revealed a large left atrial mass and a left atrial myxoma was removed at surgery. The patient remains well.

Oral flecainide, sotalol, and verapamil for the termination of paroxysmal supraventricular tachycardia.

The ability to terminate supraventricular tachycardia (SVT) acutely with an oral dose of flecainide (2.5-3.3 mg/kg), sotalol (2.0-2.9 mg/kg), and verapamil (3.3-3.7 mg/kg) was investigated in an observational study of six patients with SVT normally controlled by an antitachycardia pacemaker. The pacemaker was programmed to induce SVT and the stability of SVT was observed for 90 minutes as a baseline. Subsequent studies involved testing of the three antiarrhythmic drugs on separate occasions, given in random order as crushed tablets in orange juice during pacemaker induced SVT, with plasma drug levels collected every 15 minutes for 90 minutes post drug ingestion. Sotalol produced drug induced slowing of SVT in all six patients, with termination of SVT in three patients by 60-65 minutes, with maximum plasma levels of 0.76-2.09 micrograms/mL achieved by 90 minutes. Flecainide produced maximum plasma levels of 83-745 ng/mL, 60-90 minutes post ingestion, and slowed SVT in three patients. SVT was terminated in three patients after 45-85 minutes, but no effect on SVT was seen in two patients who had inadequate plasma levels (< or = 166 ng/mL) from doses < 3 mg/kg. Verapamil produced maximum plasma levels of 0 (undetectable) to 388 ng/mL, 45-90 minutes post ingestion, and slowed SVT in three patients, but only one of these patients reverted to sinus rhythm (at 40 min). No effect on SVT was seen in three patients due to undetectable plasma levels. We concluded that sotalol (> or = 2 mg/kg) and flecainide (> or = 3 mg/kg) appeared to be suitable oral drugs for termination of SVT.(ABSTRACT TRUNCATED AT 250 WORDS)

Placebo effect of nitrate monotherapy for myocardial ischemia.

Nitrate monotherapy was assessed by treadmill exercise stress testing in 18 patients with significant but relatively asymptomatic myocardial ischemia who were receiving no other antianginal therapy. In addition, prolonged ambulatory electrocardiographic monitoring was performed in 7 patients with demonstrable ischemia during baseline monitoring. After baseline assessment, 5 treatment periods were used in a random order (each of 1 week duration), incorporating 2 dose levels of transdermal nitrate (10 and 20 mg/24 hours) and isosorbide dinitrate (ISDN) (30 and 60 mg/day in divided doses) with a 10-hour nitrate-free interval every 24 hours, as well as a placebo period using a double-blind technique. All treatment periods (including placebo) showed a significant (p < 0.01) 45 to 69% prolongation in the time to 1 mm ST depression during exercise. Paired baseline times of 231 +/- 28 and 233 +/- 30 seconds increased to 367 +/- 37 seconds with 30 mg/day of ISDN, 393 +/- 37 seconds with 60 mg/day of ISDN, 381 +/- 31 seconds with 10 mg/day of transdermal nitrate, and 372 +/- 33 seconds with 20 mg/day of transdermal nitrate. The value for placebo was 342 +/- 29 seconds, which was not significantly different from active treatment (p > 0.1). Some patients appeared to individually respond to > or = 1 nitrate preparation significantly more than to placebo, but this appeared to be unpredictable and largely independent of dosage level and route of administration. There was a qualitatively similar but statistically insignificant reduction in total ischemic time during ambulatory monitoring.(ABSTRACT TRUNCATED AT 250 WORDS)

Beneficial effects of low dose amiodarone in patients with congestive cardiac failure: a placebo-controlled trial.

The effects of amiodarone in a low dosage (200 mg every 8 h for 2 weeks, then 200 mg/day) was assessed in a double-blind placebo-controlled trial in 34 patients with a history of severe congestive heart failure but no sustained ventricular arrhythmia. Left ventricular ejection fraction, treadmill exercise tolerance and 48 h electrocardiographic monitoring were assessed before and repeatedly after beginning amiodarone or placebo therapy over 6 months, and side effects were monitored. In patients receiving amiodarone, the ejection fraction increased significantly from 19 +/- 7 to 29 +/- 15% at 6 months (p less than 0.01 from baseline), but not significantly in 14 placebo-treated patients (18 +/- 5 to 22 +/- 9%). Exercise tolerance increased significantly in amiodarone-treated patients (median 433 s to 907 s, p less than 0.05), but not significantly in placebo-treated patients (757 to 918 s). Nonsustained ventricular tachycardia was present in 88% of amiodarone-treated patients before, but in only 21% of patients after 6 months of treatment (p = 0.06); it was seen in 43% of placebo-treated patients at baseline and in 50% after 6 months. Fifty percent of amiodarone-treated patients had side effects (principally nausea) and the drug was withdrawn in 28% of cases; no life-threatening effects were seen. Low dose amiodarone appears to have a multifaceted potential to produce benefits in arrhythmia control, exercise tolerance and ventricular function in patients with a history of severe congestive heart failure, but better control of side effects (principally nausea) appears essential. Effects on mortality could not be determined from this study; such assessment requires a larger cohort of patients.

Failure of episodic high-dose oral verapamil therapy to convert supraventricular tachycardia: a study of plasma verapamil levels and gastric motility.

The practicality of administering large oral doses of verapamil tablets to terminate supraventricular tachycardia (SVT) was investigated in 10 patients. A pilot study in four patients showed that unexpectedly low plasma levels (less than 40 ng/ml) were obtained 60 minutes after administering 160 mg or 240 mg of verapamil during SVT. Nuclear studies in the six other patients showed that fractional liquid gastric emptying times (T) were significantly prolonged in SVT compared to sinus rhythm (SR), p less than 0.05 from T 1/3 onward. Further verapamil absorption studies (200 to 360 mg) performed during SVT and SR in five of six patients showed that peak verapamil levels in four patients in SVT were 23% to 71% lower than in sinus rhythm, where they had peaked at greater than 250 ng/ml 60 minutes post verapamil ingestion, and areas under the plasma concentration time curves were 26% to 100% (mean 67%) less in SVT than in SR for all five patients. SVT was terminated by verapamil in one patient after 40 minutes and the rate of SVT was slowed after 90 minutes in two other patients. Thus plasma verapamil levels are considerably reduced during SVT as compared to SR, and changes in gastric emptying are likely a contributing cause. Since SVT was converted to sinus rhythm in only 1 of 10 patients within 1 hour, large oral doses of verapamil tablets appear unsatisfactory for the episodic treatment of SVT.

Mode of stimulation versus response: validation of a protocol for induction of ventricular tachycardia.

Electrophysiologic studies were prospectively performed in 91 consecutive patients referred for evaluation of sustained ventricular tachycardia or sudden cardiac death. Fifty-two patients had a history of sustained ventricular tachycardia and 39 patients had a history of sudden cardiac death. The identical stimulation protocol was used in all patients. The stepwise protocol involved atrial pacing, burst ventricular pacing, single, double, and triple extrastimuli during ventricular pacing. Stimulation was performed at the right ventricular apex at two and five times diastolic threshold. Using this protocol, ventricular tachycardia was inducible in 48 (92%) of the 52 patients with a history of sustained ventricular tachycardia and in 28 (72%) of 39 patients with a history of sudden cardiac death (p less than 0.02). The use of a third extrastimulus increased the yield of inducible ventricular tachycardia by 37% in patients with a history of sustained ventricular tachycardia and by 25% in patients with a history of sudden cardiac death. Stimulation at five times diastolic threshold and stimulation from the right ventricular outflow tract added a 15% increment in overall yield of inducible ventricular tachycardia in patients with a history of sustained ventricular tachycardia, and a 26% increment in yield in patients with a history of sudden cardiac death. Forty-four (92%) of the 48 inducible patients in the sustained ventricular tachycardia group had inducible monomorphic ventricular tachycardia as compared to 19 (68%) of 28 patients in the sudden cardiac death group (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Hemodynamic benefits of synchronized 1:1 atrial pacing during sustained ventricular tachycardia with severely depressed ventricular function in coronary heart disease.

The hemodynamic effects of atrial pacing were studied in 8 patients who had ventricular tachycardia (VT) during electrophysiologic testing. These patients had chronic recurrent VT associated with organic heart disease and depression of left ventricular function (ejection fraction = 0.23 to 0.35). Hemodynamic variables were recorded during sinus rhythm (58 to 103 beats/min), pacing-induced VT (133 to 214 beats/min) and synchronized 1:1 triggered atrial pacing (atrium paced, ventricle sensed and triggered mode) during VT. For the latter, the ventriculoatrial coupling interval was adjusted to produce a maximal blood pressure response; the optimal interval was observed to be between 60% and 73% of the RR interval. Mean arterial blood pressure decreased after the onset of VT (90 +/- 11 to 79 +/- 14 mm Hg, p less than 0.05) but increased again when atrial pacing was added, to 98 +/- 12 mm Hg. Cardiac index decreased during VT (2.2 +/- 0.5 to 1.8 +/- 0.5 liters/min/m2 p less than 0.05), but in each case improved by the addition of atrial pacing, to 1.9 +/- 0.5 liters/min/m2. Evidence from pressure recordings suggested that optimal atrial pacing resulted in atrial contraction in early left ventricular diastole. Thus, appropriately timed atrial pacing during VT can result in significant increases in blood pressure and a consistent increase in cardiac index. In addition to offering insight into the mechanisms of hemodynamic compromise during VT, the clinical use of this technique may be to improve hemodynamic values in patients with hemodynamically unstable VT.