Risk Stratification In Primary Prevention Research Articles

Role of lipid and lipoprotein profiles in risk assessment and therapy

Although low-density lipoprotein cholesterol (LDL-C) remains the primary target for coronary heart disease (CHD) prevention in the latest guidelines of the National Cholesterol Education Program, many individuals who have CHD do not have substantially elevated LDL-C but have derangement of other lipid fractions, most commonly low levels of high-density lipoprotein cholesterol (HDL-C). In the guidelines, HDL-C is important in risk stratification in primary prevention, influencing the need for and intensity of treatment of LDL-C, and both HDL-C and triglyceride are defined as risk factors for the metabolic syndrome, a secondary target of therapy. Triglyceride level also determines in which individuals non–HDL-C should be a secondary target of therapy. Risk assessment that takes into account the entire lipid profile will identify more high-risk individuals than evaluating LDL-C alone. Some epidemiologic data suggest that instead of measuring the cholesterol in LDL or HDL, measuring their respective apolipoproteins, apolipoprotein (apo) B-100 and apo A-I, may improve CHD risk assessment, and in some observational and interventional studies, ratios of lipids and/or apolipoproteins have been better predictors of CHD risk than levels of any one lipid fraction. Trials of lipid-modifying therapy also suggest that apolipoproteins and ratios may provide improved targets for therapy beyond LDL-C, but optimal values have not been established. Because lipid-modifying therapy affects multiple components of the lipid profile, the effect on all lipid parameters should be considered when selecting the most appropriate agent. Therapies with beneficial effects across the lipid profile would be expected to improve CHD risk reduction.

Advanced Lipoprotein Testing by Nuclear Magnetic Resonance (NMR) and Carotid Ultrasound Predict Premature Coronary Heart Disease

PURPOSE: Many individuals suffer myocardial infarction (MI) in spite of optimal to borderline cholesterol levels. Newer tests have been proposed as adjuncts to the NCEP III guidelines to improve risk stratification for primary prevention. However, many of these tests, including advanced lipoprotein testing and carotid ultrasound (CU) have not been tested in the same population, and thus their incremental value to the guidelines remains unknown.

Role of invasive EP testing in the evaluation and management of hypertrophic cardiomyopathy.

Hypertrophic cardiomyopathy (HCM) is an inheritable condition that may cause sudden death in the absence of significant symptoms or adverse morphological features. Therefore, there is a need for identification of those patients at sufficiently high risk to warrant prophylactic treatment. Risk stratification for primary prevention of sudden death has relied upon non-invasively derived markers of risk: syncope; a family history of premature sudden death; nonsustained ventricular tachycardia on Holter; abnormal blood pressure response to exercise; and severe left ventricular hypertrophy. The presence of two or more risk factors is associated with a 6-year sudden death survival rate of 72% (56-88%), justifying the consideration of prophylactic therapy. The 6-year sudden death survival rate in patients with one or no risk factors is 94% (91-98%). In these individuals the context and severity of the risk factor may guide the decision for prophylaxis; for example, a highly malignant family history carries greater justification than a large pedigree with only one sudden death. There is a need, however, for determining risk more accurately in those individuals with only one conventional risk factor. Programmed stimulation has been studied for its predictive value in primary prevention. 'Aggressive' protocols have been used and the most commonly induced arrhythmia is polymorphic ventricular tachycardia. These findings, however, are non-specific and of limited prognostic value. In addition the patients studied have been from selected high-risk populations without a low-risk cohort for comparison. Thus invasive EP studies appear to carry little advantage over non-invasive risk stratification. This is not surprising given that the mechanisms of cardiac arrest in HCM can be varied and may be modified by abnormal vascular responses and ischaemia. The relevance of invasively induced arrhythmias may therefore be limited. Other uses for electrophysiological study include the investigation and treatment of individuals with conduction disease and/or Wolff-Parkinson-White syndrome, atrial flutter and fibrillation and monomorphic ventricular tachycardia. Appropriate management may then involve radiofrequency ablation. A permanent pacemaker will be required if the atrio-ventricular node is ablated.