Cardiovascular outcomes in elderly patients randomized to angiotensin-converting enzyme inhibitor- or diuretic-based therapy for hypertension were assessed using a Prospective Randomized Open Blinded Endpoint (PROBE)-designed study in family medical practices across Australia. After 4 years of treatment, blood pressure was reduced to the same level in both groups (-261-12 mm Hg); however, there was an 11% (95% confidence interval, 0.79-1.00; p=0.05) reduction in cardiovascular outcomes and death for subjects (17% for males; 95% confidence interval, 0.71-0.97; p=0.02) randomized to the angiotensin-converting enzyme inhibitor group in comparison to the diuretic group. These findings, suggesting that angiotensin
Transmyocardial laser revascularization (TMR) has been used to treat patients with end-stage coronary artery disease since the early 1980s. Following several individual and multi-institutional investigations, prospective randomized clinical trials have demonstrated symptomatic relief for patients treated with transmyocardial laser revascularization. Two different types of lasers are being used in the clinical arena, Holmium:YAG and CO 2 . Additionally, two different methods of laser revascularization have been attempted: open surgical and catheteredbased approaches.
An inverse association between moderate alcohol consumption and vascular disease has been shown in several studies and confirmed in recent meta-analyses. Important issues remain about the relationship between alcoholic beverages and vascular disease. Among these are the differences in types of beverages, the optimal amount of alcoholic beverage intake, the individual or environmental modulation of the alcohol-related effect, and the pattern of drinking. In particular, many studies have dealt with the question of whether wine might offer a greater protection, most likely related to its nonalcoholic components. This review discusses open questions about wine and vascular disease.
Blood/injury phobia is a problem encountered commonly in clinical practice and is accompanied by syncope in about 80% of the cases. A vasovagal reaction to the sight of blood is not a specific feature of the blood phobic population per se and has been widely described in blood donors and in normal subjects viewing violent or surgical films. It may be that a dysfunctional constitutional autonomic substrate predisposes some individuals to marked vasovagal reactions. Indeed, in comparing the hemodynamic response to head-up tilt in blood phobic and normal subjects, nine of eleven blood phobic subjects experienced syncopal or pre-syncopal events. Thus, subjects with blood/injury phobia are susceptible to vasovagal syncope, even in the absence of blood or injury stimulus.
Atrial fibrillation (AF) is the most common cardiac arrhythmia, associated with a five- to six-fold increase in the incidence of stroke due almost exclusively to embolization of thrombus formed in the left atrial appendage. Whereas epidemiological data links AF to increased mortality, recent clinical trials show no improvement in outcomes with strategies designed to maintain sinus rhythm. One possible explanation for this AF paradox is that AF is a manifestation of an underlying disease process that is not addressed by current treatment strategies. Several lines of evidence suggest that oxidant stress may contribute to the atrial remodeling and the hypercoagulable state associated with AF. These alterations involve an increase in reactive oxygen species and a concomitant decrease in the bioavailability of nitric oxide. Recently, we observed this situation in the left atrial appendage. Increased oxidant stress may be central to the perpetuation of AF, and failure to address this underlying pathology may explain the lack of efficacy seen in clinical trials.
The purpose of this study was to assess a possible relationship between left atrial appendage function and plasma brain natriuretic peptide (BNP) levels in patients with nonvalvular atrial fibrillation. Tansesophageal echocardiography and plasma BNP measurement were performed in 34 consecutive patients with chronic nonvalvular atrial fibrillation (age 69±9 years). Thirteen patients with a history of thromboembolism or echographically detected thrombus (E+ group), were compared with 21 atrial fibrillation patients without complications (E- group). The E+ group patients demonstrated greater impairment of left atrial appendage velocity and higher plasma BNP levels than the E- group patients (left atrial appendage velocity, 12±6 vs. 31±17 cm/s [p<0.05]; plasma BNP, 126±53 vs. 86±45 ng/L [p<0.05]). Overall analysis of the continuous variables with multiple logistic regression analysis revealed that BNP was a significant predictor of thromboembolism. The present data suggest the usefulness of measuring plasma BNP levels in detecting patients with a high risk for thromboembolic complications in nonvalvular atrial fibrillation.
The hemodynamics of blood have a significant effect on the vascular system. Viscosity, the resistance to flow, is a major determinant of blood flow and can be directly related to cardiovascular disease. Blood viscosity, unlike plasma viscosity, is a non-Newtonian fluid that is not constant but changes depending on the shear force and shear rate of the blood. The slower the blood flow the higher the viscosity. Small lumen vessels (arterioles and capillaries), the major regulators of peripheral resistance, can be greatly affected by blood viscosity. Mediators of blood viscosity include hematocrit, red blood cell (RBC) deformability, RBC aggregation, and plasma viscosity. Serum cholesterol has been found to increase blood viscosity by increasing RBC deformability, RBC aggregation, and plasma viscosity. In this review, the authors discuss the effects of low-density lipoprotein (LDL) apheresis, a process for immediately removing massive amounts of serum cholesterol, on the vascular system. Specifically, they highlight two methods of LDL apheresis (i.e., Liposorber and HELP), which are used in the United States. Both devices can deerease LDL cholesterol by 60%-70% in 2-3 hours. They can also significantly reduce fibrinogen levels. LDL apheresis can dramatically reduce RBC aggregation, improve RBC deformation, and lower plasma viscosity-especially when fibrinogen levels are also reduced. Blood viscosity can be lowered by as much as 20% following LDL apheresis. Improved hemorheology is believed to be one of the reasons for immediate enhancement of myocardial blood flow and velocity following treatment. During acute hyperemia, when the microcirculatory system is under stress, LDL apheresis might improve vascular flow and tissue perfusion through its ability to lower blood viscosity.
The alerting reaction to the physician's visit is known to induce a blood pressure rise termed white coat effect. This phenomenon has often been associated with a clinical condition characterized by a persistently high blood pressure in the doctor's office and a persistently normal blood pressure at other times, a condition commonly referred to as isolated once hypertension or white coat hypertension. In this paper the direct and indirect methods of assessing these phenomena are briefly discussed, together with the sometimes discrepant definitions used when referring to them. The possible clinical relevance of both white coat effect and isolated office hypertension is addressed.
There is widespread recognition of the effect of drugs on prolongation of the QT interval and subsequent development of ventricular tachycardia. Although there are literature reports of adverse cardiac events of high-dose intravenous corticosteroids, the mechanism of these changes is unrecognized. The authors report a case of markedly prolonged QT and resultant ventricular tachycardia characteristic of torsade de pointes in a patient treated with high-dose intravenous steroids and ketoconazole. Based on animal studies, these changes are likely due to a decrease in outward potassium currents. Awareness of the arrhythmogenic effects of high-dose intravenous steroids should prompt electrocardiographic monitoring of these patients.
Cocaine is a commonly used drug. It has been shown to be an independent risk factor for myocardial infarction. The mechanism of cocaine-induced myocardial ischemia differs from that of the more common atherosclerotic myocardial infarction in several important ways. The treatment is different and controversial. This review summarizes the pathophysiology and the management of cocaine-induced myocardial infarction.
Nonsustained ventricular tachycardia occurs commonly in the setting of acute myocardial infarction. By 24-48 hours after the onset of acute myocardial infarction, the incidence of nonsustained ventricular tachycardia declines. When analyzed as a dichotomous variable (present or absent), the presence of nonsustained ventricular tachycardia in the first 48-72 hours of acute myocardial infarction has been shown to have no prognostic significance. However, recent data suggest that the presence of nonsustained ventricular tachycardia in the first several hours during an acute myocardial infarction has no important prognostic significance, but that nonsustained ventricular tachycardia that occurs beyond the first several hours is associated with increased mortality. The pathogenesis of the increased mortality is unknown. Treatment should focus on the use of β blockers; specific antiarrhythmic drug therapy is not recommended. Polymorphic ventricular tachycardia is an uncommon arrhythmia in the setting of acute myocardial infarction. Its presence is thought to be associated with recurrent ischemia. Treatment should focus on aggressive attempts to reduce ischemia and intravenous amiodarone administration, if necessary.
Hypercholesterolemia has been identified as an important risk factor for the development of obstructive coronary artery disease, and studies have shown that a reduction in the level of low-density lipoprotein cholesterol is associated with a reduction in cardiovascular morbidity and mortality. This paper reviews the current approach to hyperlipidemia for primary and secondary prevention of coronary disease and identifies important questions that remain to be answered.
The rise in abuse of methamphetamine is a serious concern today. This paper explores possible connections between methamphetamine abuse and heart disease. Methamphetamine's increase of catecholamine levels causes an acute increase in cardiac stress, tone, and platelet aggregation. This may lead to vascular occlusion, rupture of coronary lesions, vasoconstriction, infarction, or dilated cardiomyopathy. Hypertension and tachycardia might promote aneurysms or aortic dissection. In experimental situations, methamphetamine causes myocardial hypertrophy, atrophy, cellular disarray, edema, eosinophilic degeneration, cellular infiltration, myolysis, granulation tissue, and fibrosis. Upon cessation of methamphetamine use, most of these conditions will reverse with time. However, fibrosis will not reverse itself. Methamphetamine also damages microtubular and actin cellular structures with prolonged use. Noncardiac complications are briefly discussed. This paper also includes a review of amphetamine and 3,4-methyl-enedioxymethamphetamine (ecstasy), noting that they have similar effects on the heart. Diagnosis and treatment are also described. More research is needed to evaluate the many potential actions that methamphetamine has on the heart.
The roles of serum creatinine and uric acid as predictors of mortality and cardiovascular disease were reviewed. The authors summarized the evidence provided by prospective studies with an observational design or by post hoc analyses of outcome trials. Mildly elevated serum creatinine is associated with higher mortality and, to a lesser extent, with higher incidences of fatal and non-fatal stroke and all cardiovascular events. Hyperuricemia is also associated with increased risks of mortality and cardiovascular disease. The association between outcome and uric acid seems more evident in women than in men. Thiazide-induced increases in serum uric acid may offset the benefit of blood pressure lowering for coronary events. In conclusion, both serum creatinine and uric acid predict mortality and, to a lesser extent, cardiovascular disease. In patients with established cardiovascular disorders and in persons with other cardiovascular risk factors, serum creatinine and uric acid may be routinely measured because of the additional prognostic information. However, mass screening for raised concentrations of serum creatinine and uric acid is currently not recommended.
Clinical evidence has established that the reduction of elevated low-density lipoprotein cholesterol levels decreases coronary heart disease events and mortality. However, despite this evidence, there is concern that low-density lipoprotein cholesterol-lowering agents are underutilized in patients who would benefit the most from treatment. Statins are the most effective agents for decreasing low-density lipoprotein cholesterol and are considered to be first-line treatment for hypercholesterolemia, after diet. Statins have also been shown to decrease triglycerides in patients with hypertriglyceridemia and to slow the progression of atherosclerosis. Statin use has been associated with significant decreases in major coronary events, stroke, and total mortality, regardless of the patient's baseline cholesterol level. Coronary benefits have been demonstrated in a wide patient group, including postmenopausal women, the elderly, hyperlipidemic diabetic patients and those with acute coronary syndromes. These outcomes reduce the use of health care resources and result in favorable cost-effectiveness ratios. As a class, statins are a well tolerated, convenient, once-daily treatment, with few adverse drug interactions. Given the weight ofevidence for the clinical and economic benefits ofstatin therapy in both primary and secondary prevention of coronary heart disease, continued underutilization is inappropriate and unjustifiable.
Syncope is a common event in all age groups and all people, with multiple causes and prognoses. In young individuals without heart disease, syncope is not likely to be a harbinger of a life-threatening disorder. However, occasionally syncope can be a warning of impending sudden cardiac death, especially in those with heart disease. The young athlete with syncope shares many characteristics with the nonathlete. Foremost among these similarities are the similar physiology and pathophysiology of syncope, presyncope, and cardiac arrhythmias. The most common cause of syncope will be neurocardiogenic syncope. In those athletes with underlying heart disease, syncope may be an ominous sign. The treatment of syncope in the athlete offers some unique challenges, often in an attempt to avoid pharmacologic therapy and to maximize ability to play. Radiofrequency ablation should be offered to those athletes with conditions in which a cure is possible. Restriction of competitive athletics is necessary for those with life-threatening conditions while those with benign conditions can continue to compete.
Coronary heart disease (CHD) originates early in life and numerous studies have shown inverse associations between body size at birth and CHD in adult life. Recently it has been shown that the increased risk for CHD associated with a small body size at birth is modified by growth during childhood. The greatest risk for CHD is noted in individuals with small body size at birth and who 'catch-up' in weight and body size during childhood. An increase in body weight and body mass index during the first year of life is however associated with a reduced risk of CHD. These recent findings add to the evidence that optimizing early growth is an important area in primary prevention of CHD. There are several potential mechanisms explaining the association between a non-optimal early growth and CHD. Behavioral, physiological, hormonal and genetic factors influence growth. Although socio-economic factors influence the risk of CHD, the association between slow fetal growth and CHD is not caused by confounding socio-economic factors. Biological programming - the process whereby a stimulus during critical periods of development has long lasting or lifelong effects on metabolism - is proposed to mediate the effects between early growth and adult diseases.
Pressure recovery is an important source of discrepancy between Doppler-estimated and catheter-measured gradients in aortic stenosis. The clinical relevance of this fluid dynamic principle has not been established in pediatric patients with congenital aortic stenosis. We retrospectively measured pressure recovery in 21 patients (11 with bicuspid aortic valves). Pressure recovery was correlated with actual Doppler/catheter discrepancies (r=0.48). The correlation was significantly weaker for bicuspid valves (r=0.21) than for trileaflet valves (r=0.69). Doppler-estimated gradients were adjusted by pressure recovery calculations in 15 of 21 children for whom Doppler overestimated the catheter-measured gradients. The correlation did not change significantly with adjustment (r=0.79 vs. r=0.81). However, the mean percent difference decreased from 34%±6% to 22%±5%. Pressure recovery accounts for a significant portion of Doppler/catheter discrepancies in pediatric patients with congenital aortic stenosis.
Objective. Patients presenting to the emergency department with chest pain who are not clearly having an acute ischemic event are often admitted for observation and testing. In this observational study, we determined the effect of having access to very early myocardial perfusion imaging on the hospital course of patients presenting with chest pain. Methods. Patients presenting to the emergency department for evaluation of chest pain, which raised suspicion of coronary disease, were followed. Patients with ECG evidence of prior Q wave myocardial infarction, or an elevation of CK-MB #1, were not included in the study. Myocardial perfusion imaging (either with exercise or dipyridamole infusion) was performed at the request of the patient's cardiologist and upon laboratory availability; the protocol included an initial rest image, with exclusion from stress testing if an abnormality was seen. Two groups were followed: Group 1 (n=54) included patients who had imaging; four patients had an abnormal test and were excluded from further analysis. Group 2 (n=25) included patients in whom the imaging study was requested, but could not be done because the laboratory was unable to accommodate the test. Patients were subsequently followed for 2 years for clinical events, including death, myocardial infarction, myocardial revascularization (percutaneous transluminal coronary angioplasty or coronary artery bypass graft), as well as repeat stress testing. Results. There was no significant difference between the groups with respect to presenting characteristics or laboratory tests. The mean length of hospital stay of patients in Group 1 (13.3±1.0 hours) was significantly lower (p<0.001) than for Group 2 (50.8±6.1 hours). In addition, the mean hospital costs were significantly lower (p=0.026) in Group 1 ($1,609.96±$139.05) than for Group 2 ($2,579.79±$388.97). In Group 2, 17/25 had stress testing prior to discharge-all were negative. Follow-up of 71 of the 75 patients (95%) with a negative rest image 2 years after the conclusion of the study revealed: 1) one (1.4%) cardiac catheterization showing normal coronary arteries; 2) one (1.4%) repeat nuclear perfusion imaging study, which was negative; and 3) one (1.4%) death due to cancer. Conclusion. Very early stress myocardial perfusion imaging of selected patients presenting to the emergency department with chest pain is safe and may impact hospital length of stay and hospital costs.
