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Background: The effect of cigarette smoking on the risk of myocardial infarction (MI) has long been investigated. However, its role on the likelihood of having MI at young age has not been well understood and appreciated. We investigated whether smoking habits can discriminate young individuals with MI from age- and sex-matched controls., Methods: We enrolled 100 consecutive patients who had survived their first episode of MI before the age of 36 years and 100 age- and sex-matched controls without a history of cardiovascular disease. Smoking habits, physical activity status, body mass index and blood lipids levels were measured in all participants., Results: 96% of the patients with premature MI and 55% of the controls reported current smoking habits (p<0.001). Moreover, patients had higher levels of total cholesterol, low density lipoprotein cholesterol, triglycerides and lower levels of high density lipoprotein cholesterol (p<0.05). Multivariate logistic regression analysis showed that current smoking increased 6-fold the odds of having a MI (95% CI 1.01 to 37), after controlling for age, sex, body mass index, hypertension, diabetes, physical activity, family history of coronary heart disease and total cholesterol levels. Finally, discriminant analysis showed that pack-years of smoking was the strongest discriminator for MI among all the investigated factors (lambda-Wilks=0.85)., Conclusions: Our study suggests that cigarette smoking seems to play the most important role for having a MI in individuals under the age of 36 years.

Depression is a common comorbid condition in patients with coronary artery disease and a well-documented risk factor for recurrent cardiac events and mortality. The exact mechanisms underlying the interplay between depression and ischemic heart disease remain poorly understood and the same is true for the most effective depression treatment for cardiac patients. This review summarizes current knowledge regarding the prognostic role of depression in patients with coronary artery disease, the pathophysiologic pathways involved, and the effects of antidepressant therapy on cardiovascular disease outcomes. With recent evidence suggesting that selective serotonin reuptake inhibitors may improve survival after myocardial infarction in patients with depression, diagnosis and treatment of this co-morbidity may be essential for the clinical management of coronary artery disease.

Background: Hypercholesterolemia predisposes to coronary artery disease and causes endothelial dysfunction; some reports suggest that endothelial derived substances are involved in ischemic preconditioning., Objective: Our aim was to examine the possibility that preconditioning maybe attenuated in a clinically relevant animal model of hypercholesterolemia with atherosclerosis., Methods: Male rabbits were fed with cholesterol enriched diet and then divided into two groups (A and B) without and with preconditioning, respectively. A second series of rabbits fed a normal diet were similarly divided into two groups (C and D) without and with preconditioning, respectively. All the animals were subjected to 30 min ischemia and 180 min reperfusion. Blood samples were collected for cholesterol assessment; arterial and heart samples were harvested at the end for histopathological examination. Infarct (I) and risk areas (R) were delineated with Zn-Cd particles and TTC staining., Results: Cholesterol in groups A and B was 58.3+/-8.7 mg% at baseline and 1402+/-125 mg% at 8 weeks (P<0.0001) and in groups C and D 57.5+/-5.8 mg% before the surgical procedure. I/R% was 39. 3+/-6.3% in group A, 16.7+/-3.9% in B (P<0.01), 41.4+/-7.5% in C and 10.8+/-3.3% in D (P<0.01)., Conclusion: We conclude that preconditioning is unlikely to be attenuated by hypercholesterolemia.

Study Objectives: Pacing-induced asynchrony may deteriorate left ventricular function; however, limited data exists in humans. The aim of our study was to compare left ventricular hemodynamics during short-term atrioventricular sequential pacing from the right ventricular apex and from the outflow tract of the right ventricle., Design: Three 5-min pacing intervals were applied in a random order, at a rate of 15 beats/min above the resting sinus rate. Atrioventricular sequential pacing from the two sites was compared with atrial pacing. During each pacing mode, left ventricular pressure was recorded, and cardiac output was calculated using Doppler echocardiography., Setting: Cardiac catheterization laboratory., Patients: Twenty patients (18 male, mean age 62 +/- 11 years) without structural heart disease were studied., Results: During atrial pacing, maximum negative first derivative of pressure (dp/dt) was 1,535 +/- 228 mm Hg/s; during pacing from the apex it decreased to 1,221 +/- 294 mm Hg/s (p = 0.0001), but was not significantly different during pacing from the outflow tract (1,431 +/- 435 mm Hg/s, p > 0.05). Isovolumic relaxation time constant (tau) during atrial pacing was 39.7 +/- 11.9 ms; during pacing from the apex, it increased to 47.9 +/- 14.0 (p = 0.001), but was not significantly different during pacing from the outflow tract (42.5 +/- 11.2, p > 0.05). Peak systolic pressure decreased significantly during atrioventricular sequential pacing from either site; however, it did not differ between the two sites. No differences in end-diastolic pressure, maximum positive dp/dt, or cardiac output could be demonstrated., Conclusion: In patients with no structural heart disease, short-term right ventricular outflow tract pacing is associated with more favorable diastolic function, compared to right ventricular apical pacing.

In homozygous beta-thalassemia, the organ damage is mainly attributed to excessive iron deposition through the formation of oxygen free radicals. Despite appropriate transfusion and chelation therapy and low ferritin levels, patients still develop organ failure, heart failure being the main cause of death. This study was designed to determine whether the decreased antioxidant activity of the apolipoprotein E (APOE) 4 allele could represent a genetic risk factor for the development of left ventricular failure (LVF) in beta-thalassemia homozygotes. A total of 251 Greek beta-thalassemia homozygotes were studied. Patients were divided in three groups: group A (n = 151) with no cardiac impairment, group C (n = 47) with LVF, and 53 patients with LV dilatation and normal LV systolic function constituted the group B. DNA was obtained from all patients, and the polymerase chain reaction was used to analyze the polymorphism at the APOE locus. The APOE allele frequencies were compared with those of a Greek control sample of 216 healthy blood donors. Patients with no cardiac impairment had an APOE 4 allele frequency (7.9%) not different from population controls (6.5%, P > .05), while patients with LVF had a significantly higher frequency of APOE 4 (12.8%) than the controls (P < .05, odds ratio = 2.11, 95% confidence interval 1.03 to 4.32). The APOE 4 allele may represent an important genetic risk factor for the development of organ damage in homozygous beta-thalassemia., (Copyright 1998 by The American Society of Hematology)

Previous studies have indicated that ventricular asynchrony may significantly affect resting coronary blood flow velocity. Our study argues against this hypothesis, as comparable left anterior descending blood flow velocities were found during three pacing modalities, associated with varying degrees of asynchrony: (a) atrial pacing, (b) atrioventricular (AV) sequential pacing from the right ventricular apex and (c) AV sequential pacing from the proximal right ventricular septum.

Objective: To examine the hypothesis that an altered left ventricular depolarization sequence may augment infarct size., Methods: Twenty-one New Zealand male rabbits were anesthetized and ventilated. The chest was opened and two electrodes were placed on the right atrium and ventricle. The rabbits were then randomized to atrial (n = 7), atrioventricular (AV) sequential (n = 7) or no (n = 7) pacing. The pacing rate was 20 beats/min higher than the sinus rate. After 1 min of pacing, the left coronary artery was occluded by a snare. After 30 mins, the snare was released and pacing was stopped. After 120 mins of reperfusion the experiment was terminated. Normal areas and areas at risk were delineated, infarct size was measured and the infarcted areas and areas at risk were planimetered., Results: All results were expressed in cubic centimetres, and the ratio of the infarcted area to area at risk was calculated as a percentage (%I:R). The double product during ischemia was 21,546 +/- 2300 in controls, 23,000 +/- 3005 in rabbits with atrial pacing and 24,418 +/- 4253 in rabbits with AV pacing (F = 1.33, P = 0.28), and %I:R was 41.4 +/- 19.8, 43.9 +/- 15.4 and 38.4 +/- 18.4 (F = 0.16, P = 0.84), respectively., Conclusions: An altered left ventricular depolarization sequence in rabbit hearts does not increase infarct size.

To investigate if the response of the contralateral artery during coronary angioplasty (PTCA) is different in hypertensive than in normotensive patients and whether this response is related to plasma levels of endothelin-1 (ET-1). We examined the change in ET-1 plasma levels and the reactivity of the left circumflex artery (LCx) during PTCA of the left anterior descending branch in 10 hypertensive and 23 normotensive patients. Peripheral vein blood samples were drawn for ET-1 estimation at baseline, after the end of the first balloon inflation, at the end of PTCA, and 4 h later. Angiograms of the LCx were obtained at baseline and during the 1st balloon inflation. The ET-1 level in hypertensives increased from 6.81 +/- 3.76 at baseline to 7.54 +/- 4.76 pmol/l (P = n.s.) at the end of PTCA, while in normotensives it increased from 8.21 +/- 3.73 to 11.56 +/- 5.04 pmol/l (F = 7.48, P = 0.0002) respectively. The LCx distal segment diameter increased from 1.29 to 1.50 mm during balloon inflation in hypertensive, and from 1.44 to 1.53 mm (F = 5.03, P = 0.03) in normotensives. The diameter increase was related to the baseline ET-1 level (r = -0.67, P = 0.005) in the normotensives, but not in the hypertensives. Thus ET-1 has a weaker vasomotion effect on the coronary vasculature in hypertensives than in normotensives during PTCA.

We investigated intracoronary cyclic-guanosine monophosphate (c-GMP) levels during percutaneous transluminal coronary angioplasty (PTCA) since experimental studies have shown the endothelial origin of c-GMP production. Intracoronary c-GMP and cyclic adenosine monophosphate (c-AMP) were measured during coronary angioplasty in 24 patients with chronic coronary artery disease. Four coronary blood samples were taken through a catheter from the coronary artery the first sample before coronary angiography and the other three from distal to coronary obstruction, as follows: before the balloon inflation, at the maximum inflation and 5 min after restoration of coronary flow. c-GMP increased from 7.9 +/- 1.0 pmol/ml and 7.5 +/- 0.9 pmol/ml before angiography and balloon inflation to 11.1 +/- 1.3 pmol/ml at the maximum inflation (P < 0.01), with a trend to decrease 5 min after the end of the intervention (9.5 +/- 1.0 pmol/ml, P: NS). Intracoronary c-AMP levels remained almost unchanged. Five venous samples were taken to measure c-AMP before coronary angiography, before PTCA, and 5 min, 2 h and 24 h after PTCA. c-AMP values 2 and 24 h after PTCA (17.8 +/- 1.7 pmol/ml and 17.5 +/- 1.7 pmol/ml, respectively) were lower than the highest value (22.1 +/- 2.1 pmol/ml) found 5 min after PTCA, (P < 0.001). c-GMP increases distal to coronary obstructive lesion during PTCA at the time of balloon inflation, while c-AMP remains unchanged. c-AMP rises in venous circulation only. PTCA stimulates the mechanism of c-GMP release, while systemic c-AMP increase seems to be related to the stress occurring during catheterisation and PTCA.

Passive leg raising is commonly used for the initial treatment of hypovolemic shock. However, there are many reports which have pointed out that it does not produce significant autotransfusion effect. We tried to evaluate the effects of passive leg raising on the cardiovascular performance in coronary artery disease patients in stable condition. We studied 31 patients of 51 +/- 10 years. Two M-mode echocardiographic and continuous wave Doppler studies of aortic flow were obtained. The first was performed while the patient was lying on the left side and the second after passive leg elevation. Left ventricular end-diastolic dimension increased by 0.40 +/- 0.82 cm (P = 0.007), fractional shortening by 2.5 +/- 6% (P = 0.01), peak aortic blood velocity by 5 +/- 14 cm/s (P = 0.02), and velocity time integral by 1.7 +/- 3.0 cm (P = 0.0007). From the above it is concluded that passive leg elevation really does increase preload, and consequently cardiac performance, by the classical Frank-Staring relationship in normovolemic coronary artery disease patients.

We report a case of a 72-year-old lady with rheumatic heart disease and chronic, long-lasting atrial fibrillation, who reverted spontaneously to sinus rhythm. Doppler study showed evidence of mechanical contraction of the right but not of the left atrium. This may be a sign of marked histologic changes in the atria and may require the insertion of a permanent pacemaker, because of subsequent development of sinus bradycardia.

To find a noninvasive method for estimating left ventricular end-systolic pressure, 40 patients were studied during cardiac catheterization. Arterial pressure was taken directly from the ascending aorta. Carotid pulse tracing and measurement of blood pressure by cuff sphygmomanometry were taken simultaneously. The tracings were calibrated and left ventricular end-systolic pressure was estimated directly and indirectly. Simple linear regression analysis gave the equations: (1) left ventricular end-systolic pressure direct = 0.56 left ventricular end-systolic pressure indirect + 43.8 (r = 0.61, P = 0.00004), and (2) left ventricular end-systolic pressure direct = 0.39 systolic arterial pressure indirect + 48.8 (r = 0.62, P = 0.00002). To test the accuracy of the technique the study was continued in 40 patients. Left ventricular end-systolic pressure was also estimated by the 2 equations. Left ventricular end-systolic pressure direct was correlated with left ventricular end-systolic pressure estimated by the 2 equations and there was no statistical difference. This noninvasive technique is a bedside method for clinical measurement of left ventricular end-systolic pressure.