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The Hurst's the Heart Central Illustrations provide you with a concise view and a visual summary of the chapter quickly and clearly. We have simplified the presentation of text and data in this visual snapshot of every chapter in Hurst's the Heart.
Hurst's Central Illustration: Risk Factors for Hypertension and Risks of the Condition
Various risk factors are associated with the development of hypertension, which in turn increases the risk of the development of cerebrovascular and cardiovascular disease.
Hurst's Central Illustration: Pathophysiology of Hypertension
The pathophysiology of hypertension involves the impairment of renal pressure natriuresis, the feedback system in which high blood pressure induces an increase in sodium and water excretion by the kidney that leads to a reduction of the blood pressure. Pressure natriuresis can result from impaired renal function, inappropriate activation of hormones that regulate salt and water excretion by the kidney (such as those in the renin-angiotensin-aldosterone system), or excessive activation of the sympathetic nervous system.
Hurst's Central Illustration: Treatment of Patients with Hypertension
Treatment of patients with hypertension usually requires both lifestyle and pharmacological intervention. *In most cases; interventional therapies (such as renal denervation and baroreflex activation therapy) are being investigated for individuals with drug-resistant hypertension. †Smoking cessation does not lower blood pressure, but is important in the prevention of cardiovascular disease. ‡Choice depends on presence of concomitant disease and risk factors.
Hurst's Central Illustration: The Metabolic Syndrome
Factors that contribute to the pathogenesis, diagnosis and therapeutic strategies for metabolic syndrome. *Various guidelines require the coexistence of at least 2-3 of these factors.
Hurst's Central Illustration: Pathophysiology of Obesity and Consequential Cardiovascular Disease
Pathophysiology of obesity and consequential cardiovascular disease. Genetic, environmental, and behavioural factors all contribute to obesity. Obesity causes changes to the hypothalamic regulation of appetite that make it challenging to reduce adiposity and maintain any weight loss, and thereby promote obesity. Obesity also promotes the behavioural factors that promote obesity; for example, by causing psychological changes to food preferences (toward foods with greater caloric density with high fat and sugar content), by making physical activity more difficult, and by increasing the risk of sleep apnea and thereby impacting negatively on sleep hygiene. Obesity is also associated with alterations in adiposity-accumulation of intra-abdominal fat and of lipids within muscles and liver cells-that result in insulin resistance and dysregulated secretion of adipokines, which lead to diabetes mellitus and the metabolic syndrome, and can eventually result in the development of cardiovascular disease.
Hurst’s Central Illustration: Vascular Complications in Diabetes Mellitus and Management Strategies.
Microvascular and macrovascular complications of type 1 and type 2 diabetes mellitus. Major microvascular complications include nephropathy and retinopathy. Diabetes also significantly increases the risks of coronary heart disease and acute myocardial infarction, diabetes-related cardiomyopathy and heart failure, and stroke. Management strategies are shown in the red boxes. ACE, angiotensin-converting enzyme; HFpEF, heart failure with preserved ejection fraction; HFrEF, heart failure with reduced ejection fraction.
Hurst’s Central Illustration: Causes and Treatment of Hyperlipidemia.
Causes of hyperlipidemia (and, therefore, atherosclerotic cardiovascular disease) and treatment strategies employed. Hypercholesterolemia and hypertriglyceridemia are both types of hyperlipidemia; combined hyperlipidemia indicates an increase in concentration of both cholesterol and triglycerides. High levels of HDL-cholesterol are associated with reduced risk of atherosclerotic cardiovascular disease; however, to date, no convincing randomized controlled trial data have demonstrated that raising HDL-cholesterol levels prevents the condition.
Hurst’s Central Illustration: Pathogenesis of Smoking-Induced Cardiovascular Disease.
Pathogenesis of cigarette-smoking-induced cardiovascular disease.
Hurst’s Central Illustration: Effective Strategies for Reducing Risks of Cigarette Smoking.
Effective strategies for reducing risks (including cardiovascular risks) of cigarette smoking include addressing smoking cessation in individuals and implementing policies to reduce smoking prevalence and exposure to secondhand smoke. Screening should be incorporated into all outpatient and hospital encounters. Healthcare providers should ask if their patient smokes, advise them to quit, assess their interest in and willingness to quit, assist their patient with counseling and pharmacotherapy, and arrange follow-up appointments to monitor their patient’s progress.
Hurst’s Central Illustration: Pathophysiological Development of a Vulnerable Plaque in Atherothrombosis.
Development of an atherosclerotic plaque that becomes vulnerable to plaque rupture or erosion and, therefore, to thrombosis.
Hurst’s Central Illustration: Coronary thrombus formation.
Coronary thrombus formation following rupture of an atherosclerotic plaque. When the endothelium is damaged and the deeper layers of the vessel walls are exposed to the circulating blood, ensuing biomolecular interactions result in activation and aggregation of platelets as well as the generation of thrombin. The consequential formation of a thrombus is influenced by various local and systemic factors.
Hurst's Central Illustration: Quantifying the physiological severity of coronary artery disease for clinical decision making.
Quantifying the physiological severity of coronary artery disease for clinical decision making. Coronary flow reserve and stress perfusion are complimentary quantifiers of physiological severity of coronary artery disease that should be used together to provide a complete and definitive depiction of disease severity.
Hurst's Central Illustration: Pathogenesis, Diagnosis and Treatment of Nonobstructive Atherosclerotic and Nonatherosclerotic Coronary Heart Disease.
Hurst's Central Illustration: Acute Coronary Syndromes.
Definition of acute coronary syndromes, a term that encompasses unstable angina, non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI). Diagnosis relies on integration of information from clinical history, an initial electrocardiogram (ECG), and laboratory results. Myocardial necrosis is a necessary, but not sufficient, component of NSTEMI and STEMI. CCS, Canadian Cardiovascular Society.
Hurst's Central Illustration: Histologic Findings After Myocardial Infarction.
Timelines of histologic findings after myocardial infarction in nonreperfused and reperfused* infarctions. Myocardial salvage occurs if reperfusion takes place within 4-6 hours after onset of chest pain or electrocardiographic changes, and the infarct is likely to be subendocardial without transmural extension. *Reperfused within 4-6 hours after onset of chest pain or electrocardiographic changes.