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  • Cardiology - Cardiovascular Disease and Cancer
    2025/08/05
    Cardiovascular Disease in CancerI. Cardiotoxicity of Radiation Therapy to the ThoraxPrevalence and Significance: Radiation therapy, while improving survival in patients with thoracic malignancies (e.g., Hodgkin lymphoma, early-stage breast cancer), has led to cardiovascular disease becoming "the most common nonmalignant cause of death in patients treated with chest radiation therapy, accounting for 25% of deaths in survivors of Hodgkin lymphoma."Mechanism and Onset: Thoracic irradiation damages all cardiac cells and structures, including the "pericardium, myocardium, valves, coronary and peripheral vasculature, and conduction system." Clinical disease typically presents "two to three decades after treatment," though some manifestations can occur earlier.Increased Risk Factors: The risk of radiation-induced cardiac injury is heightened in patients receiving "concomitant anthracyclines or trastuzumab." Contemporary radiation techniques aim to "limit total dosage and field size" to decrease complications.Spectrum of Cardiovascular Diseases (Table 42):Pericardial Disease:Acute pericarditis: "Most common early manifestation," affecting 2.5% of patients.Chronic or constrictive pericarditis: Develops in "10% to 20% of patients 5 to 10 years after radiation therapy." Pericardial calcification is not always present, and late constriction can occur without prior acute pericarditis.Cardiomyopathy: Radiation damages microvasculature, leading to "endothelial dysfunction and ischemia that result in myocardial fibrosis, diastolic dysfunction, and restrictive physiology." Differentiating it from pericardial constriction is crucial for treatment.Valvular Disease: Affects all valves, predominantly left-sided. "Valvular regurgitation due to tissue retraction is the most common valvular lesion in the first two decades after therapy," evolving to "mixed regurgitation and stenosis" with later fibrosis and calcification.Conduction Defects: Common in long-term survivors, including "atrioventricular block, bundle branch block." Increased need for permanent pacing after valve replacement surgery in irradiated patients.Coronary Artery Disease (CAD): Occurs "earlier and with increased incidence." Lesions are typically "ostial, long, smooth, and concentric and have higher fibrotic content than typical atherosclerotic lesions." Traditional risk factors (smoking, dyslipidemia, hypertension) exacerbate incidence, requiring aggressive management.Surgical Outcomes: Surgical outcomes for radiation-associated cardiovascular disease are "significantly worse than in matched cohorts." Percutaneous approaches, such as percutaneous aortic valve replacement, "may be preferable" for aortic stenosis in this group.Surveillance and Prevention:No consensus on cardiac testing in asymptomatic patients, but "baseline evaluation including echocardiography is reasonable."Some organizations recommend "stress echocardiography at 5 to 10 years after completion of therapy or at age 30 years, whichever comes first."Serum biomarkers, nuclear medicine testing, and coronary CT are "not recommended" for routine screening.Statins, ACE inhibitors, and aldosterone antagonists have "not been proved to prevent radiation-induced cardiovascular disease," despite their role in risk factor reduction.II. Cardiotoxicity of ChemotherapyGeneral Principles: Chemotherapy can cause "reversible or dose-dependent, irreversible cardiac injury" (Table 43). Strategies to minimize risk include optimizing traditional risk factors and identifying high-risk patients (Table 44) before treatment.Key Cardiotoxic Agents and Effects (Table 43 & associated text):Left Ventricular Dysfunction (LVD):Anthracyclines (Doxorubicin, Epirubicin, Idarubicin):Acute toxicity: Rare (<1%), reversible, presenting as heart block, arrhythmias, heart failure, myocarditis, or pericarditis.Chronic progressive toxicity: Typically irreversible, presenting as dilated cardiomyopathy. "Most closely linked with doxorubicin."Onset: Early (within 1 year) in 1.6% to 2.1%; late (after 1 year) in up to 5%.Dose-dependent: "Late-onset chronic progressive toxicity is related to total cumulative dose." Incidence of heart failure up to 26% at 550 mg/m2 doxorubicin, with clinical evidence appearing "10 to 20 years after treatment."Mitigation strategies: Dexrazoxane (iron chelator) for high-risk patients; continuous infusion vs. bolus; liposomal formulations of doxorubicin. ACE inhibitors, ARBs, and beta-blockers have not been proven to prevent toxicity.Trastuzumab: Causes "LV systolic dysfunction, with symptoms of heart failure in 3% to 7% of patients." More common in patients older than 50 and with concomitant anthracycline use. Toxicity often reversible.Other Agents: Alkylating agents (cyclophosphamide, ifosfamide), antimicrotubular agents (paclitaxel, docetaxel), proteasome inhibitors (bortezomib, carfilzomib), tyrosine kinase inhibitors (sunitinib).Ischemia: Antimetabolites (5-fluorouracil, capecitabine), antimicrotubular ...
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    32 分
  • Cardiology - Cardiomyopathies in Pregnancy
    2025/08/05
    Cardiovascular DiseaseExecutive SummaryThis briefing document summarizes key information regarding cardiovascular health during pregnancy, drawing insights from "Pregnancy and Cardiovascular Disease - Cardiovascular Medicine Text - MKSAP 19.pdf". It highlights the increasing maternal mortality in the US due to cardiovascular disorders, the physiological changes during normal pregnancy, and the critical importance of prepregnancy evaluation, multidisciplinary management, and careful consideration of medication and anticoagulation therapies for women with pre-existing or pregnancy-related cardiovascular conditions. Special attention is given to high-risk conditions like peripartum cardiomyopathy and Marfan syndrome.I. Maternal Mortality Trends and Primary CausesMaternal mortality in the United States has increased over the past two decades, a trend contrasting with decreasing rates in other Western countries. The leading cause of maternal mortality is acquired cardiovascular disorders, specifically "cardiomyopathy, coronary artery disease, and aortic disorders."II. Cardiovascular Changes During Normal PregnancyUnderstanding normal physiological changes is crucial for distinguishing between healthy and pathologic signs. Key cardiovascular adaptations during a normal pregnancy include:Relative Anemia: Due to a greater increase in plasma volume compared to erythrocyte mass.Decreased Mean Arterial Pressure: Resulting from "reduced systemic vascular resistance and increased heart rate and cardiac output."Increased Heart Rate and Cardiac Output: Maternal cardiac output "peaks at approximately 40% to 50% above the prepregnancy level by the 32nd week," and can further increase to "as much as 80% above the prepregnancy level" during delivery.Common Normal Symptoms/Signs: Mild dyspnea, dyspnea with exertion, atrial and ventricular premature beats, heart rate increased by 20-30%, modest blood pressure decrease (~10 mm Hg), and a "basal systolic murmur grade 1/6 or 2/6 present in 80% of pregnant patients, S3."Table 45 (Normal Versus Pathologic Signs and Symptoms in Pregnancy) provides a detailed comparison, distinguishing normal physiological changes from symptoms like orthopnea, chest pain, atrial fibrillation, heart rate >100/min, high blood pressure (≥140/90 mm Hg), systolic murmur grade ≥3/6, or any diastolic murmur/S4, which are considered pathologic.III. Prepregnancy Evaluation and Risk StratificationMandatory Prepregnancy Counseling: "All women with cardiovascular disease should receive pregnancy counseling," including genetic counseling and testing if appropriate. Multidisciplinary Approach: A comprehensive evaluation involving a "cardiologist, a maternal-fetal medicine specialist, and an obstetric anesthesiologist" is essential to assess risks and formulate a management plan for labor and postpartum. Risk Assessment Tool: The modified World Health Organization pregnancy risk classification is currently the "most accurate system of risk assessment."A. Low-Risk ConditionsWomen with certain conditions generally experience no increased morbidity or mortality:Uncomplicated small patent ductus arteriosusMild pulmonary stenosisMitral valve prolapseSuccessfully repaired simple lesions (atrial or ventricular septal defect, patent ductus arteriosus, anomalous pulmonary venous drainage)Isolated atrial or ventricular ectopic beatsTetralogy of Fallot, most supraventricular arrhythmias, and Turner syndrome without aortic dilatation. These patients can typically be managed and deliver in a local hospital.B. Extremely High-Risk Conditions (Require Expert Center Care)Conditions conferring "extremely high risk for maternal mortality or severe morbidity" necessitate care and delivery at "an expert center for pregnancy and cardiac disease":Pulmonary hypertensionPrevious peripartum cardiomyopathy with residual left ventricular dysfunctionSevere left ventricular dysfunction (ejection fraction <30% or NYHA functional class III-IV symptoms)Severe mitral stenosisSymptomatic severe aortic stenosisMarked ascending aorta dilatationIV. Management of Cardiovascular Disease During PregnancyA. Valvular LesionsObstructive: Symptoms may arise due to increased blood volume/cardiac output; intervention before pregnancy should be considered.Regurgitant: Generally well-tolerated during pregnancy.B. Hypertrophic CardiomyopathySymptomatic obstructive hypertrophic cardiomyopathy: Treated with "nonvasodilating β-blockers, with monitoring of fetal growth."C. ArrhythmiasMost arrhythmias are benign.Shared decision-making is crucial for antiarrhythmic drugs, considering maternal and fetal risks/benefits.Most β-blockers (except atenolol) are safe for pregnancy and breastfeeding.Adenosine is the drug of choice for acute symptomatic supraventricular tachycardia.Amiodarone is rarely used due to toxicity.D. Delivery MethodVaginal delivery is generally preferred due to "less blood loss, quicker recovery, and lower risk for thrombosis."Cesarean delivery...
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    37 分
  • Cardiology - Congenital Disease
    2025/08/05
    Adult Congenital Heart Disease (ACHD)Date: October 26, 2023Purpose: This briefing document summarizes key themes, important ideas, and facts regarding Adult Congenital Heart Disease (ACHD) based on the provided source material.Executive SummaryMedical and surgical advancements have led to a growing population of adults with congenital heart disease (CHD). This demographic requires specialized, multidisciplinary care due to common cardiovascular "residua" from previous interventions. The document highlights various specific CHD conditions, including Patent Foramen Ovale (PFO), Atrial Septal Defect (ASD), Ventricular Septal Defect (VSD), Patent Ductus Arteriosus (PDA), Pulmonary Stenosis (PS), Aortic Coarctation, and Tetralogy of Fallot (TOF), detailing their pathophysiology, clinical presentation, diagnostic evaluation, treatment, and post-closure follow-up. A significant theme across all conditions is the importance of specialized cardiology follow-up, careful consideration of activity restrictions, and comprehensive reproductive health counseling, especially regarding pregnancy risks and contraception. Additionally, the document addresses the unique challenges and management strategies for patients with cyanotic CHD, including Eisenmenger syndrome, emphasizing the need for highly specialized care for these complex cases.Main Themes and Key Insights1. Growing ACHD Population and the Need for Specialized Care: * Key Fact: "Medical and surgical advances have resulted in more adults than children with congenital heart disease (CHD) in North America." * Importance: This highlights a fundamental shift in patient demographics, necessitating a focus on adult-specific management strategies and long-term care. * Implication: The specialized nature of ACHD management underscores the "importance of periodic follow-up by a team ideally consisting of the internist and a cardiologist trained in adult CHD." * Specifics: "Specialized care is critical for patients born with complex and cyanotic congenital cardiac disease, symptomatic patients, and patients who desire pregnancy."2. Comprehensive Patient Counseling and Holistic Care: * Reproductive Health: "Patients with CHD should be offered reproductive health counseling." This includes discussions on contraception, balancing its use against pregnancy risks, and pre-pregnancy counseling for those on anticoagulation due to associated "maternal and fetal risks." * Psychological Well-being: "Anxiety and depression are prevalent but underrecognized in patients with CHD, and screening for these mood disorders should be a routine aspect of care." This emphasizes a holistic approach to patient management beyond purely cardiac issues. * Infectious Disease Prevention: Hepatitis C screening is recommended, and Hepatitis B vaccination is advised for non-immune individuals.3. Common Cardiovascular Residua and Long-Term Follow-up: * General Principle: "Cardiovascular residua are common in patients with previous intervention for congenital cardiac lesions." This necessitates lifelong monitoring. * Condition-Specific Examples: * ASD: Atrial fibrillation risk persists after closure, and "Rare complications after device closure include device migration, erosion into the pericardium or aorta, and sudden death." * VSD: "Residual or recurrent VSD, arrhythmias, PH, endocarditis, and valve regurgitation are recognized complications following VSD closure." * PS: "Patients with previous PS intervention (balloon or surgical) often have severe pulmonary regurgitation; thus, long-term clinical and TTE follow-up is recommended." * Aortic Coarctation: "Following coarctation repair, hypertension occurs in up to 75% of patients and should be treated." * TOF: "Severe long-standing pulmonary regurgitation causes right heart enlargement, tricuspid regurgitation, exercise limitation, and both atrial and ventricular arrhythmias and is the most common reason for reoperation after TOF repair." The incidence of sudden cardiac death after TOF repair is "approximately 2% per decade."4. Condition-Specific Management Strategies:* **Patent Foramen Ovale (PFO):** * **Diagnosis:** Typically by transesophageal echocardiography (TEE) with color flow Doppler or agitated saline injection. * **Treatment:** Antiplatelet therapy for embolic stroke of undetermined source. PFO closure is recommended for patients under 60 with embolic-appearing infarcts and no other stroke mechanism, offering a "3.4% at 5 years" recurrent stroke risk reduction, but with a "3.9%" periprocedural complication rate and increased atrial fibrillation risk (0.33% per year). No treatment is needed for asymptomatic, incidentally detected PFO. * **Associated Conditions:** Platypnea-orthodeoxia syndrome and Atrial Septal Aneurysm (ASA), which "reportedly increases the risk for stroke compared with PFO alone."* **Atrial Septal Defect (ASD):** * **Types:** Ostium secundum (most common), ostium primum, sinus venosus, and coronary ...
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    1 時間 12 分
  • Cardiology - Peripheral Arterial Disease
    2025/08/05
    Peripheral Arterial DiseaseI. Overview and EpidemiologyPeripheral Artery Disease (PAD) is primarily characterized by the narrowing of the aortic bifurcation and arteries of the lower extremities, including the iliac, femoral, popliteal, and tibial arteries. The most common cause is atherosclerosis. PAD is a significant health concern, considered a "coronary heart disease risk equivalent," meaning both asymptomatic and symptomatic patients face an elevated risk for ischemic events such as myocardial infarction, stroke, and cardiovascular death. Early detection is crucial for risk factor modification.Key Facts:Definition: Narrowing of arteries, predominantly in the lower extremities, due to atherosclerosis.Prevalence: Incidence increases from age 40, reaching approximately 10% by age 70.Gender Differences: Occurs later in life for women but has a higher overall prevalence in women due to their longer lifespan.Cardiovascular Risk: PAD is a "coronary heart disease risk equivalent," placing patients at high risk for myocardial infarction, stroke, and cardiovascular death.Risk Factors:Smoking (current or past)Diabetes mellitusHypertensionHyperlipidemiaIncreasing ageFamily history of atherosclerosisScreening Guidelines (AHA/ACC):Screening with an Ankle-Brachial Index (ABI) is "reasonable in asymptomatic persons" with specific risk factors:Age 65 years or older.Age 50-64 years with atherosclerosis risk factors (e.g., smoking, diabetes, hypertension, dyslipidemia) or family history of PAD.Age younger than 50 years with diabetes and one additional atherosclerosis risk factor.Known atherosclerotic disease in another vascular bed (coronary, carotid, subclavian, renal, or mesenteric artery stenosis, or abdominal aortic aneurysm).Note: The U.S. Preventive Services Task Force finds insufficient evidence to support routine ABI screening for lower extremity PAD.II. Clinical PresentationPAD presents with a wide spectrum of clinical manifestations, as it is defined by an abnormal ABI rather than solely by symptoms.A. Intermittent Claudication (IC)Description: "Exertional leg pain relieved by rest."Symptoms: Cramping, tightness, aching, fatigue in buttock, hip, thigh, calf, or foot, consistent walking distance at onset, not occurring with standing still, relief within <5 minutes by standing or sitting.Progression: Most patients have stable symptoms, but approximately 25% worsen, and 10-20% undergo revascularization within 5 years.Complications: Annual risk for myocardial infarction, stroke, or cardiovascular death is approximately 5% to 7%.B. Atypical Exertional Leg PainPatients may experience pain that does not fit the classic description of claudication.C. Asymptomatic PADDefined solely by an abnormal ABI value without noticeable symptoms.D. Chronic Limb-Threatening Ischemia (CLTI) / Critical Limb IschemiaSeverity: The "most severe form of PAD," affecting fewer than 5% of patients.Manifestations: Ischemic rest pain, tissue ulceration, and gangrene.Ulcer Characteristics: Commonly on distal toes, plantar aspect of the foot, anterior lower leg, or trauma sites. Usually painful with "sharply demarcated borders with a dry, pale gray or yellow wound base without evidence of granulation tissue."Prognosis: High rates of major amputation (30%) and mortality (20%) within 1 year of diagnosis.Treatment: Surgical or endovascular revascularization is usually necessary for limb salvage.III. EvaluationA comprehensive evaluation, including history, physical examination, and diagnostic testing, is essential for suspected PAD.A. History and Physical ExaminationHistory: Inquire about walking impairment, claudication vs. pseudoclaudication (see Table 38 for distinguishing characteristics), skin breakdown, foot ulcers, and education on foot protection.Physical Exam Components (Table 39):Measure blood pressure in both arms (difference >15 mm Hg suggests subclavian stenosis).Auscultate for arterial bruits (e.g., femoral artery).Palpate for abdominal aortic aneurysm.Palpate and record pulses (radial, brachial, carotid, femoral, popliteal, posterior tibial, dorsalis pedis).Evaluate for elevation pallor and dependent rubor of foot.Inspect feet for ulcers, fissures, calluses, tinea, and tendinous xanthoma; evaluate overall skin care.Distinguishing CLTI: Differentiate CLTI from chronic venous disease (leg edema, pigmented/brawny induration of gaiter zone, shin/ankle ulceration).B. Diagnostic TestingAnkle-Brachial Index (ABI):Description: "The most commonly used diagnostic modality" for lower extremity PAD, measuring the ratio of lower extremity to upper extremity systolic blood pressures.Guidelines: Recommended for "all patients with history or physical examination findings suggestive of PAD."Advantages: Simple, inexpensive, noninvasive, sensitivity/specificity approaching 90%.Procedure: Measure blood pressures in both arms and at dorsalis pedis and posterior tibial ankle locations. ABI for each leg is calculated as the higher ankle pressure ...
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    27 分
  • Cardiology - Aortopathies
    2025/08/05
    Aortic Diseases: A Comprehensive BriefingDate: October 26, 2023Purpose: This briefing document provides a detailed overview of various aortic diseases, including chronic conditions like aneurysms and acute, life-threatening syndromes such as dissection and rupture. It consolidates key information on definitions, causes, risk factors, symptoms, diagnosis, surveillance, and treatment strategies, drawing from provided medical sources.1. Introduction to Aortic DiseasesAortic diseases encompass a spectrum of conditions affecting the aorta, the body's largest artery. These conditions range from chronic issues like thoracic and abdominal aortic aneurysms and aortic atheromas to acute, highly perilous events such as aortic dissection and aneurysm rupture. Prompt diagnosis, appropriate treatment, and vigilant surveillance are crucial for preventing disease progression, complications, and mortality.2. Thoracic Aortic Aneurysm (TAA)2.1. Definition and CharacteristicsTAA is defined as an increase in the thoracic aortic diameter greater than 50% relative to the expected or normal dimension, which varies by age, sex, and body type. TAAs can occur at the aortic root, ascending aorta, aortic arch, or descending aorta, most commonly affecting the root and ascending aorta, often linked to atherosclerosis.2.2. Causes and Risk FactorsCystic medial degeneration: The primary cause, involving weakening of the aortic wall due to loss of smooth muscle fibers and elastic fiber degeneration.Connective tissue disorders: Common in patients younger than 50 years, including Marfan syndrome, Ehlers-Danlos syndrome, and Loeys-Dietz syndrome.Bicuspid aortic valve: A significant risk factor, occurring in approximately 50% of affected individuals.Other risk factors: Hypertension, smoking, and advanced age.Other listed causes: Atherosclerosis, other genetic/congenital conditions (e.g., Turner syndrome, coarctation of the aorta), vasculitis (e.g., Takayasu arteritis, Giant cell arteritis), infectious causes (e.g., septic embolism, syphilis), and prior aortic injury or acute aortic syndrome.2.3. SymptomsTAAs are frequently asymptomatic and detected incidentally. When symptoms occur, they may include:Infrequent: Dysphagia (difficulty swallowing) and hoarseness due to compression of surrounding structures.Rupture: Severe chest pain, back pain, sudden shortness of breath, or sudden death.Associated with aortic regurgitation: Diastolic heart murmur, wide pulse pressure, or symptoms of heart failure.2.4. Diagnosis and SurveillanceScreening: Recommended only for patients with known genetic conditions predisposing to aortic aneurysms and dissections (e.g., Marfan syndrome, Ehlers-Danlos syndrome), or a family history of TAA or aortic dissection.Imaging Modalities (Table 36):Transthoracic echocardiography (TTE): Good for aortic root/proximal ascending aorta; no radiation/contrast. Limited visualization of distal ascending aorta, arch, and branches.Transesophageal echocardiography (TEE): Excellent visualization from root to descending aorta; no radiation/contrast. Invasive, operator dependent.CT angiography (CTA): Visualizes entire aorta and side branches; rapid; high sensitivity/specificity. Exposes patient to radiation and iodinated contrast.Magnetic resonance angiography (MRA): Visualizes entire aorta and side branches; high sensitivity/specificity; no radiation. Prolonged acquisition, contraindications (pacemakers, defibrillators, some kidney disease).Aortography: Provides exact information on size/shape of aortic lumen and side branches. Invasive, requires dye, potential for nephrotoxicity and worsening dissection. Poor for intramural hematoma.Measurement: Aortic diameter should be measured perpendicular to the long axis.Surveillance Frequency:3.5 to 4.4 cm diameter: Annual imaging.4.5 to 5.4 cm diameter: Imaging every 6 months.Marfan syndrome: Repeat assessment 6 months after initial diagnosis, then annually if stable.Rapid expansion (>0.5 cm/year) or approaching repair threshold: More frequent imaging.2.5. TreatmentMedical Therapy:For TAAs <5.0 cm.Aggressive blood pressure control: Goal <130/80 mm Hg.β-Blockers: Preferred antihypertensive agents; associated with reduced aneurysm growth, especially in Marfan syndrome.Losartan: Also associated with reduced aneurysm growth in Marfan syndrome.Surgical Repair: Warranted to prevent rupture, the leading cause of death in TAA patients.Degenerative ascending aortic aneurysm: >5.5 cm in diameter or rapid growth (≥0.5 cm/year or ≥0.3 cm/year over 2 years).Sporadic aneurysms: 5.0 cm or larger may be considered.Nonsyndromic hereditary TAA: ≥4.5 cm with high-risk family history; ≥5.0 cm without high-risk family history.Marfan syndrome/genetically mediated disorders: Lower threshold for elective repair (4.0-5.0 cm).Bicuspid aortic valve with ascending aortic aneurysm: >5.5 cm, or 5.0 cm if additional dissection risk factors or low operative risk.Concomitant cardiac surgery: Aortic repair should be ...
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    25 分
  • Cardiology - Pericardial Disease
    2025/08/04
    Pericardial Disease Briefing Document1. Acute PericarditisDefinition: Acute pericarditis is the inflammation of the pericardium, the fibrous sac surrounding the heart.Key Characteristics & Diagnosis (at least two of four criteria):Chest Pain: Typically "sharp, severe, and positional." It is worse when supine and improves with sitting up and leaning forward. Unlike angina, it is "not exacerbated by exertion nor relieved by rest or nitroglycerin."Pericardial Friction Rub: A "hallmark of acute pericarditis," described as a "harsh, scratchy sound" with classically three components corresponding to atrial systole, ventricular systole, and ventricular filling. It is not affected by respiration, differentiating it from a pleural rub.ECG Changes: "Concave ST-segment elevation in multiple leads" that does not follow a single coronary artery distribution. "PR-segment depression in lead II or reciprocal PR-segment elevation in lead aVR" may also be present. This contrasts with acute myocardial infarction ECG findings.New Pericardial Effusion: Presence of fluid around the heart. The absence of an effusion, however, "does not exclude acute pericarditis."Causes (most often idiopathic or presumed viral):Infectious: Viral (Enterovirus, herpesvirus, adenovirus, parvovirus), Bacterial (Mycobacterium tuberculosis, Pneumococcus spp., Staphylococcus spp.), Fungal.Noninfectious: Autoimmune diseases, Cancer (metastatic lung/breast cancer, melanoma, lymphoma, leukemia), Metabolic conditions (uremia, myxedema), Drug-related (hydralazine, procainamide), Iatrogenic (cardiac surgery - postpericardiotomy syndrome, coronary perforation, pacemaker lead penetration), Other (irradiation, aortic dissection). Tuberculosis is a significant concern in endemic areas and specific patient populations.Evaluation Support:Echocardiography: Used to evaluate for pericardial effusion.CMR imaging/Gated Cardiac CT: Identifies "pericardial inflammation, characterized by pericardial thickening and late gadolinium enhancement."Serologic Evidence: Elevated erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and leukocytosis. Serum cardiac troponin levels may be "normal or may be slightly elevated if there is a component of myopericarditis."Management:Outpatient vs. Hospitalization: Most managed as outpatients, but hospitalization is required for high-risk features like temperature >38°C, subacute onset, large effusion/tamponade, oral anticoagulation, or lack of response to treatment.First-line Therapy: Aspirin (750-1000 mg every 8 hours for 1-2 weeks) or NSAIDs (ibuprofen 600 mg every 8 hours for 1-2 weeks).Adjunctive Therapy: "Colchicine (0.5 mg once or twice daily for 3 months) is recommended as adjunctive therapy to shorten symptom duration and reduce treatment failure and recurrence."Glucocorticoids: Reserved for specific cases (recurrent, incessant, or chronic pericarditis despite standard therapy; uremic pericarditis unresponsive to dialysis; contraindications to NSAIDs; autoimmune-mediated pericarditis). Prednisone is added to standard therapy. CRP can guide tapering.Activity Restriction: Athletes should not return to competitive exercise for 3 months. Non-athletes restrict strenuous activity until symptoms resolve.2. Pericardial Effusion and Cardiac Tamponade2.1. Pericardial EffusionDefinition: Accumulation of fluid within the pericardial space. Causes: Often idiopathic, but malignancy, infections (tuberculosis in endemic areas), autoimmune disease, hypothyroidism, and iatrogenic causes should be considered. Management:Pericardiocentesis: Considered for diagnostic and therapeutic purposes if cancer or bacterial infection is suspected, or for large idiopathic effusions of >3 months' duration (due to 1 in 3 patients progressing to tamponade).Empiric Treatment: Reasonable for effusions of unknown cause with elevated inflammatory markers.2.2. Cardiac TamponadeDefinition: "Cardiac tamponade occurs when fluid accumulation within the pericardial space compresses the heart and impedes diastolic filling." It can arise rapidly with low volumes (trauma, aortic dissection) or slowly with large volumes (neoplastic disease, hypothyroidism).Clinical Presentation & Evaluation:Signs: Tachycardia, muffled heart sounds, and elevated central venous pressure (CVP). Hypotension may occur as pressures rise. The "y descent of the jugular venous pulse may be absent."Pulsus Paradoxus: A "key clinical feature," characterized by a "fall in systolic pressure of greater than 10 mm Hg during inspiration." It is not specific to tamponade.ECG: Sinus tachycardia, "electrical alternans (related to a swinging motion of the heart within the pericardial fluid)," or low voltage.Chest Radiography: "Typically enlarged cardiac silhouette (water bottle heart)" if fluid accumulated slowly.Echocardiography: Essential for diagnosis, defining fluid presence, distribution, and volume. Key findings include "Early diastolic collapse of the right ventricle, late diastolic collapse ...
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    23 分
  • Cardiology - Cardiomyopathies
    2025/08/04
    Myocardial Disease1. Hypertrophic Cardiomyopathy (HCM)1.1 Overview and Clinical PresentationDefinition: HCM is an "autosomal dominant heritable disorder related to mutations in the genes that primarily encode sarcomeric proteins." It is characterized by increased left ventricular (LV) wall thickness without other underlying causes (e.g., hypertension).Prevalence: Affects approximately "1 in 500 persons" and can be identified in all age groups, though "index cases typically present within the third to fourth decades of life" in the U.S.Asymptomatic Nature: "Most patients with HCM are asymptomatic and have normal life expectancy," often diagnosed during evaluation for a heart murmur or abnormal ECG.Symptomatic Presentation: Symptomatic individuals typically present with "signs and symptoms of heart failure (dyspnea, fatigue) or arrhythmias (palpitations, syncope)."Sudden Cardiac Death (SCD): SCD "may be the initial manifestation in some patients."Pathophysiology of Symptoms: Heart failure symptoms are due to "abnormal LV filling (diastolic dysfunction)" and "dynamic left ventricular outflow tract (LVOT) obstruction."Diastolic Dysfunction: Involves "increased chamber stiffness, progressive fibrosis, and myocardial ischemia."Dynamic LVOT Obstruction: The "classic form of HCM," characterized by "asymmetric LV hypertrophy with prominent interventricular septal thickening." Found in 30% of patients at rest and an additional 40% with provocation."Eject-obstruct-leak" triad: During systole, "anterior motion of the mitral valve results in early to midsystolic obstruction of the LVOT and subsequent mitral regurgitation related to leaflet malcoaptation."1.2 EvaluationPhysical Examination: May be normal without LVOT obstruction. A cardiac murmur is common with LVOT obstruction. Dynamic maneuvers (Valsalva, standing from squat, peripheral pulse after PVC) help differentiate HCM from fixed valvular aortic stenosis (see Table 27 in original source).Murmur Characteristics: Ejection-quality, usually best heard at the left lower sternal border, "generally does not radiate to the carotid arteries."Valsalva Maneuver: "Increase in intensity of murmur during strain phase."ECG: Abnormal findings in 75% to 95% of patients, including "increased QRS voltage, evidence of left atrial enlargement, LV conduction abnormalities, pathologic Q waves, and significant repolarization abnormalities."Echocardiography (TTE): Most common diagnostic tool. Demonstrates hypertrophy (≥15 mm LV region or 13-14 mm with first-degree relative with HCM), LVOT obstruction, and mitral regurgitation. Provocative maneuvers (Valsalva, squatting) and exercise echocardiography may be used.Cardiac Magnetic Resonance (CMR) imaging: Indicated for inconclusive echocardiographic findings to clarify diagnosis. Useful for differentiating HCM from other conditions causing increased LV wall thickness.Ambulatory ECG Monitoring: "24- to 48-hour ambulatory ECG monitoring should be performed to evaluate for arrhythmias." Nonsustained ventricular tachycardia indicates higher SCD risk.Exercise Stress Testing: Reasonable for functional status and prognostic information.Differential Diagnosis (Table 28): Must differentiate from other conditions with increased LV wall thickness like "Hypertension," "Athlete heart," "Amyloidosis," "Fabry disease," and "Friedreich ataxia."1.3 Risk Stratification and ManagementAnnual Mortality Risk: "Patients with HCM have an annual risk for death of 1%, primarily related to fatal arrhythmia and heart failure."SCD Risk Factors (Table 29):Previous SCD or sustained ventricular tachycardiaLV wall thickness ≥30 mm≥1 Episode of syncope thought to be arrhythmic in natureLV apical aneurysmLVEF <50%Implantable Cardioverter-Defibrillator (ICD):Secondary Prevention: Recommended for patients with previous SCD or sustained ventricular tachycardia.Primary Prevention: "Reasonable" for patients with one or more established risk factors.CMR in Risk Assessment: Beneficial for assessing maximum LV wall thickness, ejection fraction, LV apical aneurysm, and extent of myocardial fibrosis with late gadolinium enhancement (LGE). LGE ≥15% can serve as a risk modifier for ICD placement in indeterminate cases.Lifestyle Interventions: For overweight/obese patients, weight loss to decrease LVOT obstruction, heart failure, and atrial fibrillation risk. Avoid dehydration, excessive alcohol, and exposures causing vasodilation/decreased preload (e.g., saunas, hot tubs).Exercise: "Mild- to moderate-intensity exercise is generally safe and beneficial." Athletes require comprehensive evaluation and shared decision-making.Pharmacologic Therapy for Symptomatic Patients:First-line: Nonvasodilating β-blockers (avoid carvedilol, labetalol, nebivolol).Alternatives: Verapamil or diltiazem if β-blockers are contraindicated/intolerated.Persistent Symptoms with LVOT Obstruction: Adding a cardiac myosin inhibitor or disopyramide.Caution with Diuretics: Use cautiously for dyspnea, ...
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    26 分
  • Cardiology - Vavulopathies
    2025/08/04
    Valvular Heart Disease1. SummaryValvular Heart Disease (VHD) is a significant cardiac condition affecting approximately 20 million people in the United States, primarily age-dependent. It involves structural or functional valve abnormalities leading to either regurgitation (failure to close competently) or stenosis (failure to open effectively). VHD progression is slow, often causing patients to unconsciously limit activity, emphasizing the need for careful history and detailed physical examination. Diagnosis relies on ECG, chest radiography, and transthoracic echocardiography (TTE), with classification into four stages (A-D) to guide monitoring and intervention. While medical therapy offers symptom palliation, surgical or transcatheter interventions are crucial for improving long-term survival, especially in severe cases. A multidisciplinary "heart team" approach is recommended for intervention considerations. Specific VHDs discussed include Aortic Stenosis, Aortic Regurgitation, Bicuspid Aortic Valve Disease, Mitral Stenosis, Mitral Regurgitation, Tricuspid Valve Disease, and conditions related to Prosthetic Valves and Infective Endocarditis (IE).2. General Principles of Valvular Heart Disease (VHD)Definition and Prevalence: VHD is characterized by cardiac dysfunction due to "structural or functional valve abnormalities resulting from failure of the valves to either competently close (regurgitation) or effectively open (stenosis)." It affects around 20 million people in the U.S., with prevalence increasing with age (3-6% in those ≥65 years).Clinical Presentation: Patients often "limit their activity unconsciously in response" to slow progression. "Exertional dyspnea is the most common symptom," accompanied by others such as angina, syncope, palpitations, and edema, depending on lesion and severity.Diagnosis and Evaluation: Essential tests include "Twelve-lead ECG, chest radiography, and transthoracic echocardiography (TTE)."Staging: VHD is classified into four stages (A-D) based on risk factors, symptoms, lesion severity, ventricular response, pulmonary/systemic circulation effects, and rhythm changes (Table 22):Stage A (At risk): Patients with VHD risk factors.Stage B (Progressive and asymptomatic): Asymptomatic with progressive VHD.Stage C (Asymptomatic severe): Asymptomatic with severe VHD, categorized by compensated (C1) or decompensated (C2) ventricular function.Stage D (Symptomatic severe): Patients with VHD-related symptoms.Management Philosophy: "Medical therapy, although often effective for symptom palliation, has not been shown to prevent VHD progression or improve long-term survival." Surgery is "life-saving in select patients," requiring careful surgical risk calculation (age, morbidities, frailty, procedure-specific impediments). A "multidisciplinary approach with a heart team consisting of a cardiologist, a surgeon, and an interventional cardiologist is recommended" for intervention.3. Specific Valvular Heart Diseases3.1. Aortic Stenosis (AS)Etiology: Most commonly "degeneration of the valve that occurs with aging," or congenital (bicuspid aortic valve). Rheumatic disease and chest irradiation are other acquired causes.Pathophysiology: Chronic pressure overload of the left ventricle (LV) leads to concentric LV hypertrophy, myocardial interstitial fibrosis, diastolic dysfunction, and eventual systolic heart failure.Symptoms & Prognosis: "Exertional dyspnea, syncope, and angina are the most common symptoms," often not appearing until severe. "Among asymptomatic patients with severe aortic stenosis, 75% will die or develop symptoms within 5 years. Once symptoms occur, life expectancy is generally only 1 to 2 years."Diagnosis: TTE is the primary imaging modality. Severe AS is typically defined by "a small valve area (≤1.0 cm2), high peak velocity (>4 m/s), and/or high mean gradient (>40 mm Hg)." Subsets like low-flow, low-gradient AS require further evaluation (dobutamine echocardiography).Management: "Aortic valve replacement is a life-prolonging procedure." Indications include symptoms, LV systolic dysfunction (<50% ejection fraction) in asymptomatic patients, or concomitant cardiac surgery.Surgical Aortic Valve Replacement (SAVR) vs. Transcatheter Aortic Valve Implantation (TAVI): Both have similar survival rates (1-3% operative mortality). Choice depends on symptoms and surgical risk. TAVI is recommended for symptomatic patients >80 years or younger patients with life expectancy <10 years, and for high/prohibitive surgical risk patients with good post-procedure survival prospects. For 65-80 years, either is appropriate with shared decision-making.Medical Therapy: Statins are ineffective in slowing progression. Guideline-directed medical therapy is for coexistent hypertension or heart failure, with caution for vasodilators.3.2. Aortic Regurgitation (AR)Etiology: Can be acute or chronic, stemming from aortic root pathology or valve pathology (e.g., endocarditis, bicuspid valve, ...
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