Decrease in coronary blood flow reserve during hyperlipidemia is secondary to an increase in blood viscosity.

BACKGROUND: During maximal hyperemia, capillaries provide the greatest resistance to flow. A major determinant of capillary resistance is viscosity. We, therefore, hypothesized that abnormal coronary blood flow (CBF) reserve observed during hyperlipidemia is secondary to increased blood viscosity and not abnormal coronary vasomotion. METHODS AND RESULTS: Maximal hyperemia was induced in 9 dogs using adenosine. Serum triglyceride levels were increased by incremental doses of Intralipid. A good correlation was noted between serum triglyceride levels and blood viscosity (r=0.82). Neither total coronary blood volume nor myocardial blood volume changed with increasing serum triglyceride levels, indicating lack of vasomotion. Myocardial vascular resistance (MVR) increased with increasing triglyceride levels (r=0.84), while hyperemic myocardial blood flow (MBF) decreased (r=-0.64). The decrease in hyperemic MBF was associated with a decrease in blood velocity (r=-0.56). These findings were confirmed with direct intravital microscopic observations in the mice cremaster muscle. CONCLUSIONS: Increasing lipid levels in a fully dilated normal coronary bed causes no change in large or small vessel dimensions. Instead, the increase in blood viscosity causes capillary resistance to rise, which attenuates hyperemic CBF. Therefore, the abnormal CBF reserve associated with hyperlipidemia is due to increase blood viscosity and not abnormal vascular function.

Switching to statins: a challenge for primary care.

In 1997, doctors in England received official guidelines on the use of statins (3-hydroxy-3-methylglutaryl coenzyme A inhibitors) for primary and secondary prevention of coronary heart disease (CHD). Six months later we determined the status of patients who had been discharged from a specialist lipid clinic in 1989. 195 patients received questionnaires, with the consent of their general practitioners, regarding morbidity in, the subsequent decade and present medication, and were asked to have their cholesterol checked. Analysis was confined to the 86 with a current cholesterol measurement. Of 61 patients who had been discharged on a regimen of dietary advice and/or medication for primary prevention of CHD, 8 had been changed to a statin and 6 had been started on one. According to the new guidelines, none of these qualified for treatment. Of 25 patients who had been discharged on drugs for secondary prevention, all qualified for a statin but only 14 were receiving one--in 6 cases without achieving the recommended reductions in cholesterol. In many of the patients reviewed, treatment had not been altered to conform with the new guidelines. If hyperlipidaemic patients are to benefit promptly from advances in treatment, one solution might be a central registry that arranged regular tests and reported back to general practitioners. However, since many patients at risk do not have very high cholesterol levels, a coordinated approach to CHD risk factors would be preferable.

Vasovagal syncope: a new treatment for an old problem.

Vasovagal syncope is an extremely common condition that is most often benign. However, in some individuals it can be far more severe, with frequent, sudden, and prolonged episodes of loss of consciousness. The effects can be traumatic, not only from the acute event but from the lifestyle changes that are necessitated by these attacks. We report on the presentation and diagnosis of once such individual and discuss the various treatment options. In addition, supported by recently published evidence, we demonstrate how a pacemaker with rate-drop response is an effective form of treatment.

Vasculitis masquerading as aortic valve endocarditis.

Small vessel vasculitis and endocarditis can both present with multisystem involvement and may present a diagnostic dilemma. Renal and cardiac involvement is common in small vessel vasculitis and rarely small vessel vasculitis may cause heart block. When a patient presents with diffuse symptoms, deteriorating renal function, and heart block, endocarditis and vasculitis should be included in the differential diagnosis. The case is discussed of a man with a history of aortic valve endocarditis who presented again with similar symptoms, deteriorating renal function, and heart block. There was no evidence of aortic valve endocarditis with abscess formation. A renal biopsy confirmed small vessel vasculitis and the patient responded promptly to immunosuppressive treatment. Correct diagnosis is essential in such cases, as immunosuppression in true endocarditis can be catastrophic. In this case, with the correct diagnosis, immunosuppression proved life saving and prevented erroneous aortic valve surgery.

Arrhythmogenic right ventricular dysplasia. An illustrated review highlighting developments in the diagnosis and management of this potentially fatal condition.

Arrhythmogenic right ventricular dysplasia is an inherited, progressive condition. Characterised by fatty infiltration of the right ventricle, it frequently results in life threatening cardiac arrhythmias, and is one of the important causes of sudden cardiac death in the young. There are characteristic electrocardiographic and echocardiographic features that all physicians need to be aware of if we are to reduce these occurrences of premature death. Diagnosis with magnetic resonance imaging is discussed along with current treatment options.

Anthracycline-induced cardiomyopathy.

Anthracycline cardiomyopathy is less frequently encountered nowadays, due to the well-recognised dose limitations and cardiac monitoring protocols used by chemotherapy centres. However, it is a condition that will persist due to the sensitivity of some patients to these drugs and the necessity for large doses to be used for certain individuals. We have demonstrated the benefit of angiotensin-converting enzyme inhibitor therapy and would consider introducing these compounds at the earliest opportunity. The use of probucol and vitamins as antioxidants capable of preventing the onset of cardiomyopathy in humans appears to require further investigation but may significantly reduce the incidence of this condition in the future.

Detection of apical hypertrophic cardiomyopathy by cardiovascular magnetic resonance in patients with non-diagnostic echocardiography.

OBJECTIVE: To investigate the role of cardiovascular magnetic resonance (CMR) in a series of patients with ECG repolarisation changes and normal echocardiography. PATIENTS AND DESIGN: 10 patients with anterolateral T wave inversion for which there was no obvious pathological cause who had normal routine echocardiography without contrast for the exclusion of hypertrophic cardiomyopathy (HCM) also had CMR that was diagnostic of apical HCM. RESULTS: Apical HCM detected by CMR could be morphologically severe with wall thickness up to 28 mm, or mild. The extent of repolarisation abnormalities did not correlate to the morphological severity. CONCLUSIONS: In patients with unexplained repolarisation abnormalities, a normal routine echocardiogram without contrast does not exclude apical HCM. Further imaging with CMR or contrast echocardiography may be required. The reliance on routine echocardiography to exclude apical HCM may have led to underreporting of this condition.