Aortic dissection is a life-threatening acute aortic syndrome characterized by a tear in the aortic intimal layer, which allows blood to flow into the medial layer and create a false lumen that can propagate along the aortic length. This condition can rapidly lead to fatal aortic rupture, vital organ malperfusion, or cardiac tamponade. It is universally classified by the Stanford system: Type A (involving the ascending aorta, ~60-70% of cases) and Type B (limited to the descending aorta, ~30-40% of cases).

• Etiology: Chronic hypertension is the most prevalent risk factor (present in >70% of patients), followed by connective tissue disorders (Marfan syndrome, Ehlers-Danlos syndrome), bicuspid aortic valve, aortic atherosclerosis, prior aortic surgery, traumatic aortic injury, cocaine use, and pregnancy.
• Clinical Manifestations: The hallmark symptom is sudden, severe, tearing/ripping chest or back pain. Type A dissection may be accompanied by syncope, heart failure, cardiac tamponade, myocardial infarction, or neurological deficits. Type B dissection often presents with interscapular back pain, with potential complications including lower extremity malperfusion, renal failure, or mesenteric ischemia. Untreated Type A dissection has a 1-2% hourly mortality rate, with up to 20% of patients dying before reaching the hospital.
• Diagnosis: Contrast-enhanced computed tomography angiography (CTA) is the first-line imaging modality, with >95% sensitivity and specificity to define dissection type, tear location, false lumen propagation, and organ malperfusion. Transthoracic echocardiography (TTE) is used for rapid bedside screening of Type A dissection, while transesophageal echocardiography (TEE) and magnetic resonance angiography (MRA) are used for select cases.

• Emergency Initial Stabilization: The cornerstone of all acute AD management is urgent blood pressure and heart rate control to reduce aortic wall shear stress. Targets are systolic blood pressure (SBP) of 100-120 mmHg and heart rate <60 bpm, achieved with intravenous beta-blockers (first-line), with additional vasodilators if needed. Intravenous opioids are used for pain control to reduce sympathetic activation.
• Stanford Type A Dissection: Emergency open surgical intervention is the gold standard and absolute indication, as medical management alone carries a >90% 30-day mortality rate. Procedures include ascending aortic replacement, aortic root replacement (Bentall procedure) for root involvement, and hemiarch/total arch replacement with the frozen elephant trunk technique for arch extension.
• Stanford Type B Dissection: Treatment is stratified by risk:
  • Uncomplicated Type B: Initial optimal medical therapy (OMT) with lifelong strict blood pressure control and serial surveillance is first-line.
  • Complicated Type B (malperfusion, refractory pain, high rupture risk): Thoracic Endovascular Aortic Repair (TEVAR) is the first-line minimally invasive treatment, with open surgery reserved for anatomically unsuitable cases.
• Chronic AD: Lifelong strict SBP control (<120 mmHg) is mandatory for all patients, with serial imaging surveillance. Endovascular or surgical intervention is indicated for progressive aortic dilation (>55 mm), rapid growth (>5 mm/year), or persistent symptoms.

Aortic stenosis is the most prevalent valvular heart disease in elderly adults, characterized by progressive narrowing of the aortic valve orifice, which causes left ventricular outflow tract obstruction, elevated left ventricular pressure, and eventual left ventricular hypertrophy, heart failure, and sudden cardiac death. It is classified by etiology: calcific degenerative AS (~80% of adult cases), congenital bicuspid aortic valve (BAV)-related AS (~10-15% of cases), and rheumatic AS (still prevalent in developing regions).

• Etiology: Degenerative calcific AS is driven by age-related atherosclerotic processes, including lipid accumulation, inflammation, and progressive leaflet calcification. BAV, the most common congenital heart defect, causes accelerated stenosis onset 10-20 years earlier than tricuspid aortic valves. Rheumatic AS results from post-rheumatic fever commissural fusion and scarring.
• Clinical Manifestations: Early AS is asymptomatic for decades. The classic symptomatic triad includes exertional dyspnea (heart failure), angina pectoris, and syncope. Symptomatic severe AS has a 50% 2-year mortality rate without intervention, with advanced disease presenting with severe heart failure, arrhythmias, and sudden cardiac death.
• Diagnosis: TTE is the first-line gold standard, quantifying aortic valve area (AVA), mean transvalvular gradient, peak jet velocity, and left ventricular structure and function. Severe AS is defined as AVA <1.0 cm², mean gradient ≥40 mmHg, or peak velocity ≥4.0 m/s. Cardiac CTA and TEE are used for pre-procedural planning for transcatheter intervention.

• Conservative Management: Indicated for asymptomatic mild-moderate AS, with serial echocardiographic surveillance (every 1-5 years based on severity), cardiovascular risk factor modification, and comorbidity management. No medical therapy has been proven to halt or reverse calcific AS progression.
• Surgical Aortic Valve Replacement (SAVR): The historical gold standard for severe symptomatic AS in low-to-moderate surgical risk patients, involving sternotomy, cardiopulmonary bypass, and replacement with a mechanical or bioprosthetic valve. SAVR has a 30-day mortality rate <2% in low-risk patients, with excellent long-term outcomes.
• Transcatheter Aortic Valve Replacement (TAVR): A minimally invasive catheter-based procedure (most commonly transfemoral access) that eliminates the need for sternotomy or cardiopulmonary bypass. Initially for inoperable/high-risk patients, TAVR is now the first-line guideline-recommended treatment for severe symptomatic AS across all risk strata.
• Balloon Aortic Valvuloplasty (BAV): A palliative procedure for temporary hemodynamic stabilization in critically ill patients, or as a bridge to TAVR/SAVR, with limited long-term efficacy due to rapid restenosis.

Atrial fibrillation is the most common sustained cardiac arrhythmia globally, characterized by disorganized, rapid atrial electrical activation, resulting in loss of atrial contraction, irregular ventricular response, and elevated risk of thromboembolism, heart failure, and stroke. It is classified by duration: paroxysmal AF (terminates spontaneously within 7 days), persistent AF (lasts >7 days), long-standing persistent AF (>12 months), and permanent AF (no further rhythm control attempts).

• Etiology: Common risk factors include advanced age, hypertension, coronary artery disease, heart failure, valvular heart disease, diabetes mellitus, obesity, obstructive sleep apnea (OSA), hyperthyroidism, excessive alcohol intake, and genetic predisposition.
• Clinical Manifestations: Common symptoms include palpitations, exertional dyspnea, fatigue, dizziness, and chest discomfort. Up to 30% of patients are asymptomatic (silent AF), with the first presentation being stroke or heart failure. AF is associated with a 5-fold increased stroke risk, 3-fold higher heart failure risk, and 2-fold higher all-cause mortality.
• Diagnosis: The gold standard is a 12-lead ECG showing absent consistent P waves, irregularly irregular RR intervals, and chaotic atrial activity. For paroxysmal AF, ambulatory monitoring (Holter, implantable loop recorder) is used for detection. TTE assesses structural heart disease, left atrial size, and left ventricular function, with additional testing including thyroid function and OSA screening.

• Stroke Prevention: The cornerstone of AF care, with risk stratification via the CHA₂DS₂-VASc score. Oral anticoagulation (OAC) is recommended for men with a score ≥2 and women ≥3. First-line options for non-valvular AF are non-vitamin K antagonist oral anticoagulants (NOACs), with warfarin used for valvular AF or NOAC contraindications. Left atrial appendage closure (LAAC) is a recommended alternative for patients with long-term OAC contraindications.
• Rate Control: For all AF patients, targeting a resting heart rate <80 bpm for symptomatic patients and <110 bpm for asymptomatic patients with preserved left ventricular function. First-line medications include beta-blockers, non-dihydropyridine calcium channel blockers, and digoxin for heart failure or hypotension. Atrioventricular node ablation with pacing is reserved for refractory cases.
• Rhythm Control: For patients with persistent symptoms despite optimal rate control, to restore and maintain sinus rhythm. Options include electrical cardioversion, antiarrhythmic drugs (AADs), and catheter ablation (first-line guideline-recommended therapy for symptomatic paroxysmal and persistent AF, with superior efficacy to AADs). The gold standard ablation procedure is pulmonary vein isolation (PVI) via radiofrequency or cryoballoon ablation.
• Risk Factor Modification: Critical for long-term management, including strict blood pressure control, diabetes management, weight loss, OSA treatment, alcohol cessation, and regular exercise.

Coronary artery disease, also known as ischemic heart disease, is the leading cause of death globally. It is characterized by atherosclerotic plaque buildup in the epicardial coronary arteries, causing reduced myocardial blood flow, myocardial ischemia, and potentially myocardial infarction (MI) and sudden cardiac death. It is classified into chronic coronary syndrome (CCS) (stable angina, ischemic cardiomyopathy) and acute coronary syndrome (ACS) (unstable angina, non-ST elevation MI (NSTEMI), ST elevation MI (STEMI)).

• Etiology: The primary cause is coronary atherosclerosis, driven by non-modifiable risk factors (advanced age, male gender, genetic predisposition) and modifiable risk factors (hypertension, dyslipidemia, diabetes mellitus, smoking, obesity, sedentary lifestyle, excessive alcohol intake, chronic stress).
• Clinical Manifestations:
  • Stable CCS: Classic exertional angina pectoris (retrosternal chest pressure/pain radiating to the jaw, shoulder, or arm, precipitated by exertion and relieved by rest/nitroglycerin). Some patients present with atypical symptoms (dyspnea, fatigue, epigastric pain) or silent ischemia.
  • ACS: Unstable angina presents with rest pain, new-onset severe angina, or accelerating angina. MI presents with severe persistent chest pain (>20 minutes) unrelieved by nitroglycerin, accompanied by dyspnea, diaphoresis, nausea, syncope, or cardiac arrest.
• Diagnosis: Initial evaluation includes 12-lead ECG (critical for STEMI diagnosis) and cardiac troponin (gold standard for MI diagnosis). Non-invasive testing includes stress testing and coronary CTA. Invasive coronary angiography (ICA) is the gold standard for definitive stenosis assessment and revascularization planning.

• Optimal Medical Therapy (OMT): The cornerstone of all CAD management, including:
  • Antiplatelet therapy: Lifelong aspirin for all CAD patients, P2Y12 inhibitors for ACS or post-percutaneous coronary intervention (PCI), with dual antiplatelet therapy (DAPT) for guideline-specified durations.
  • Lipid-lowering therapy: Statins, ezetimibe, and PCSK9 inhibitors, with a target LDL-C <1.4 mmol/L for very high-risk patients.
  • Antianginal therapy: Beta-blockers, nitrates, calcium channel blockers, ranolazine, and ivabradine.
  • Secondary prevention: RAAS inhibitors, strict glycemic control, and risk factor modification.
• Myocardial Revascularization: Indicated for refractory symptoms despite OMT, high-risk anatomy, or ACS.
• PCI: The first-line minimally invasive procedure, involving balloon angioplasty and drug-eluting stent (DES) implantation. Primary PCI is the gold standard for STEMI, with a target door-to-balloon time <90 minutes.
• Coronary Artery Bypass Grafting (CABG): The gold standard surgical procedure, recommended for left main disease, 3-vessel disease, or diabetes, with superior long-term survival vs. PCI in high-risk groups. Minimally invasive and off-pump CABG are widely used to reduce trauma.

Mitral valve disease encompasses two primary pathological conditions of the left atrioventricular valve: mitral stenosis (MS) and mitral regurgitation (MR), which often coexist. MS is characterized by narrowing of the mitral valve orifice, impairing left ventricular filling and elevating left atrial pressure. MR is characterized by incomplete leaflet closure, causing retrograde systolic blood flow from the left ventricle to the left atrium, leading to left ventricular volume overload and eventual heart failure.

• Etiology:
  • Mitral Stenosis: Over 90% of global cases are caused by rheumatic heart disease (RHD), from post-rheumatic fever scarring, thickening, and commissural fusion of valve leaflets and chordae. Rare causes include congenital stenosis, degenerative calcific MS, and carcinoid syndrome.
  • Mitral Regurgitation: Classified into primary (organic) MR (structural valve abnormalities: myxomatous degeneration/mitral valve prolapse, RHD, infective endocarditis, chordal rupture) and secondary (functional) MR (left ventricular dilation/dysfunction from ischemic heart disease or cardiomyopathy).
• Clinical Manifestations:
  • MS: Early symptoms include exertional dyspnea, palpitations, and fatigue. Advanced disease presents with orthopnea, paroxysmal nocturnal dyspnea, hemoptysis, atrial fibrillation (present in ~50% of patients), right heart failure, and thromboembolic stroke. Severe MS is defined as mitral valve area <1.0 cm².
  • MR: Acute MR (chordal rupture, papillary muscle infarction) presents with sudden severe dyspnea, pulmonary edema, and cardiogenic shock. Chronic MR is asymptomatic for decades, with progressive exertional dyspnea, fatigue, palpitations, and eventual left ventricular dysfunction and heart failure.
• Diagnosis: TTE is the first-line gold standard, assessing valve morphology, stenosis/regurgitation severity, left atrial size, left ventricular function, and pulmonary pressure. TEE is used for pre-procedural planning for transcatheter intervention and surgical repair.

• Mitral Stenosis Management:
  • Conservative Management: For asymptomatic mild-moderate MS, with serial surveillance, diuretics for symptom control, heart rate control for AF, and lifelong anticoagulation for AF or prior thromboembolism. Rheumatic fever prophylaxis is mandatory for all rheumatic MS patients.
  • Percutaneous Mitral Balloon Commissurotomy (PMBC): First-line treatment for symptomatic severe rheumatic MS with favorable valve morphology, a minimally invasive transseptal procedure with a >95% procedural success rate.
  • Surgical Treatment: Indicated for severe MS unsuitable for PMBC, severe MS with moderate-severe MR, or left atrial thrombus despite anticoagulation. Procedures include mitral valve repair (select cases) and mitral valve replacement (MVR).
• Mitral Regurgitation Management:
  • Conservative Management: For asymptomatic mild-moderate MR with preserved left ventricular function, with serial surveillance, guideline-directed medical therapy (GDMT) for underlying heart failure/ischemia.
  • Surgical Treatment: Gold standard for severe primary MR, with mitral valve repair (MVRp) strongly preferred over replacement for superior long-term survival and left ventricular preservation. Minimally invasive surgery is widely used.
  • Transcatheter Mitral Valve Intervention (TMVI): Minimally invasive procedures for high-risk/inoperable patients. Transcatheter edge-to-edge repair (TEER, MitraClip) is the most established, guideline-recommended for inoperable severe primary MR and selected secondary MR patients.

Cardiac tumors are rare neoplasms of the heart and pericardium, classified into primary cardiac tumors (extremely rare, originating from cardiac tissue) and secondary metastatic cardiac tumors (20-40 times more prevalent, from distant primary cancers). Primary tumors are further divided into benign (~75% of primary tumors) and malignant (~25% of primary tumors).

• Etiology and Classification:
  • Benign Primary Tumors: The most common is myxoma (~50% of all primary tumors, 75% located in the left atrium), followed by lipoma, papillary fibroelastoma, rhabdomyoma (most common in children), fibroma, and hemangioma. Complete surgical resection is curative.
  • Malignant Primary Tumors: The vast majority are sarcomas (angiosarcoma, undifferentiated pleomorphic sarcoma, leiomyosarcoma), with rare primary cardiac lymphoma. These are highly aggressive, with a poor prognosis.
  • Secondary Metastatic Tumors: Most commonly originate from lung, breast, esophageal, hematological, melanoma, and gastrointestinal cancers.
• Epidemiology: Primary cardiac tumors have an annual incidence of ~0.0017-0.028% in the general population, with an autopsy prevalence of ~0.02-0.05%. China has the world's largest cardiac tumor patient population, with an estimated 10,000-15,000 new primary cases diagnosed annually.
• Clinical Manifestations: Symptoms are highly variable and non-specific, often mimicking common cardiovascular diseases. The three primary clinical syndromes are:
  • Obstructive symptoms: Exertional dyspnea, syncope, chest pain, heart failure, or sudden death from intracavitary tumor blood flow obstruction.
  • Systemic/embolic symptoms: Constitutional symptoms (fever, weight loss, fatigue), elevated inflammatory markers, and thromboembolic events (~30-40% of myxoma patients).
  • Arrhythmic/pericardial symptoms: Atrial/ventricular arrhythmias, heart block, pericardial effusion, or cardiac tamponade.
• Diagnosis: TTE is the first-line screening modality, identifying tumor location, size, mobility, and hemodynamic impact. TEE provides superior visualization of small tumors and attachment sites. Cardiac MRI is the gold standard for tissue characterization. Endomyocardial biopsy provides histopathological confirmation.

• Benign Primary Tumors: Complete surgical resection is the gold standard and curative treatment, indicated for all symptomatic tumors and asymptomatic tumors with high embolic/obstructive risk. Resection is performed via sternotomy or minimally invasive thoracoscopic/robotic approaches, with a near 100% cure rate and <5% recurrence rate for myxoma.
• Malignant Primary Tumors: Requires a multidisciplinary comprehensive approach, including surgery, chemotherapy, radiotherapy, targeted therapy, and immunotherapy. Complete surgical resection is attempted for localized non-metastatic disease. For unresectable/metastatic disease, palliative systemic therapy is used to relieve symptoms and prolong survival. The prognosis remains poor, with a median overall survival of 6-12 months for advanced disease.
• Secondary Metastatic Tumors: Treatment is palliative, focused on managing the primary malignancy and relieving cardiac symptoms. Systemic therapy for the primary cancer is the mainstay, with local interventions including pericardiocentesis/window for malignant effusion/tamponade, surgical resection for isolated symptomatic metastases, and radiotherapy for local symptom control.
• Supportive Care: Guideline-directed management of heart failure, arrhythmias, thromboembolism, and pericardial complications.