1,722,124 research outputs found
Interaction between predisposing genes and environmental risk factors in cardiovascular disease: how prevention can counteract this salty combination
No full textN/
Treatment of heart failure: the dawn of the era of sodium-glucose co-transporter-2 inhibitors
No full textN/
Acute Coronary Syndromes: The Way Forward From Mechanisms to Precision Treatment
No full textWell into the 21st century, we still triage acute myocardial infarction on the basis of the presence or absence of ST-segment elevation, a century-old technology. Meanwhile, we have learned a great deal about the pathophysiology and mechanisms of acute coronary syndromes (ACS) at the clinical, pathological, cellular, and molecular levels. Contemporary imaging studies have shed new light on the mechanisms of ACS. This review discusses these advances and their implications for clinical management of the ACS for the future. Plaque rupture has dominated our thinking about ACS pathophysiology for decades. However, current evidence suggests that a sole focus on plaque rupture vastly oversimplifies this complex collection of diseases and obscures other mechanisms that may mandate different management strategies. We propose segmenting coronary artery thrombosis caused by plaque rupture into cases with or without signs of concomitant inflammation. This distinction may have substantial therapeutic implications as direct anti-inflammatory interventions for atherosclerosis emerge. Coronary artery thrombosis caused by plaque erosion may be on the rise in an era of intense lipid lowering. Identification of patients with of ACS resulting from erosion may permit a less invasive approach to management than the current standard of care. We also now recognize ACS that occur without apparent epicardial coronary artery thrombus or stenosis. Such events may arise from spasm, microvascular disease, or other pathways. Emerging management strategies may likewise apply selectively to this category of ACS. We advocate this more mechanistic approach to the categorization of ACS to provide a framework for future tailoring, triage, and therapy for patients in a more personalized and precise manner
Clinical implications of inflammation for cardiovascular primary prevention.
No full textWhile many questions remain unanswered in this challenging arena, the emerging status of biomarkers of inflammation provides an excellent illustration of how application of basic and clinical science of inflammation can lead to advances in clinical care. Yet we need to do better. We need to improve the number needed to treat. We should strive for further refinements in risk prediction to individualize interventions. Imaging and genetic biomarkers will likely find their place in clinical practice alongside traditional risk factors and biomarkers of inflammation in the years to come. We must aim to assure that individuals targeted for statin therapy do not lessen their adherence to a healthy lifestyle, believing that they enjoy pharmacological protection from unhealthy behaviours. At the other extreme, we need to counsel carefully certain patients to avoid creating a cohort of 'cardiac neurotics' with above median high-sensitivity C-reactive protein readings. We need to understand more about the mechanisms and clinical significance of unwanted actions of statins, including dysglycaemia. We need to devise measures to optimize lifestyle change at both a medical and societal level. For our individual patients, implementation of sustained lifestyle change has proved very challenging in practice, given the multiplicity of behaviours that require vigilance. The clinical use of biomarkers of inflammation may provide the practitioner with a tool to help gauge residual risk, and chart a course for its optimal management
Elevated troponin in stable coronary artery disease: The sound of silence
No full textNo Abstract availabl
- …
