Health
Excel
Cardiovascular Diseases Dataset – Heart & Circulatory Conditions Database
Cardiovascular Diseases Dataset
The Cardiovascular Diseases Dataset is a structured medical database containing a comprehensive list of heart and circulatory system disorders.
Cardiovascular diseases are among the leading causes of death globally, affecting the heart, blood vessels, and circulatory system. This dataset provides organised information about these conditions to support research, healthcare analytics, and application development.
Each record includes key clinical details such as disease descriptions, affected systems, symptoms, severity levels, and typical treatment approaches.
The dataset has been cleaned and structured for easy integration into spreadsheets, databases, and data analysis platforms.
It is suitable for medical researchers, healthcare developers, educators, and data scientists who need structured cardiovascular health data.
Dataset Contents
The dataset includes fields such as:
- Disease / Condition Name
- Description
- Affected Area (Heart, Arteries, Veins, Circulatory System)
- Common Symptoms
- Severity Level
- Disease Category
- Risk Factors
- Treatment Approach
Example Conditions Included
- Coronary Artery Disease
- Hypertension (High Blood Pressure)
- Heart Failure
- Atrial Fibrillation
- Stroke
- Peripheral Artery Disease
- Deep Vein Thrombosis (DVT)
- Atherosclerosis
- Cardiomyopathy
- Arrhythmia
...and many more cardiovascular conditions.
Data Preview
12 columns
25 rows shown
| No. | Disease Name | Category | Primary Cause / Etiology | Prevalence | Age of Onset | Key Symptoms | Affected Cardiovascular Structure | Diagnostic Method | Treatment Approach | Prognosis | ICD-10 Code | |
|---|---|---|---|---|---|---|---|---|---|---|---|---|
| 1 | ▸ CORONARY ARTERY DISEASES (14 disorders) | |||||||||||
| 2 | 1 | Acute Coronary Syndrome (ACS) | Coronary Artery Diseases | Umbrella term for acute myocardial ischemia; plaque rupture, erosion, or hemorrhage with superimposed thrombosis; encompasses STEMI, NSTEMI, and unstable angina; endothelial disruption activates coagulation cascade | ~1.5 million ACS events annually in US; leading cause of emergency cardiac admissions; ~800,000 MIs per year; 15-20% present as sudden cardiac death | Mean age 65-70 years; younger in males (55+ vs 65+ for females); 10% occur in patients <45 years; young ACS often associated with cocaine, hypercoagulable states, or familial dyslipidemia | Acute chest pain or pressure >20 minutes; radiation pattern varies; associated symptoms: diaphoresis, nausea, dyspnea, anxiety; atypical presentations in 30% of women, elderly, diabetics; can present with syncope, acute heart failure, or cardiac arrest | Coronary arterial system; acute plaque pathology; thrombus formation; downstream myocardial ischemia or infarction; microvascular dysfunction | ECG within 10 minutes of arrival; serial high-sensitivity troponin at 0 and 1-3 hours (0/1h or 0/3h algorithm); HEART score for risk stratification; echocardiography for wall motion; coronary angiography for definitive diagnosis | Oxygen if SpO2 <90%; morphine for refractory pain; nitroglycerin sublingual/IV; aspirin 325mg immediate; P2Y12 inhibitor; anticoagulation; primary PCI for STEMI; early invasive strategy for high-risk NSTEMI; fibrinolysis if PCI not available; secondary prevention with DAPT, statin, beta-blocker, ACEi | Depends on type and treatment timing; STEMI mortality 5-7% with PCI; NSTEMI in-hospital mortality 3-5%; overall 1-year mortality 8-12%; GRACE score predicts 6-month mortality; complete revascularization improves outcomes | I24.9 |
| 3 | 2 | Coronary Artery Aneurysm | Coronary Artery Diseases | Localized dilation >1.5x normal segment diameter; atherosclerosis (50% of adult cases); Kawasaki disease (major pediatric cause); connective tissue disorders; post-PCI; vasculitis; mycotic/infectious; iatrogenic from atherectomy | Incidence 0.3-5% on coronary angiography; giant aneurysms (>8mm) rare (<0.02%); Kawasaki disease causes in ~25% of untreated children; male-to-female ratio 2-4:1 in adults | Atherosclerotic: 50-70 years; Kawasaki disease: childhood onset (6 months-5 years) with persistence into adulthood; post-PCI: any age; connective tissue: 20-40 years | Often asymptomatic (incidental finding); may present with ACS from thrombosis or distal embolization; angina; dyspnea; rarely rupture with hemopericardium; fistula formation causing continuous murmur | Epicardial coronary arteries; RCA most commonly affected in adults (40%); LAD (32%); LCx (23%); aneurysmal dilation with disruption of media; intraluminal thrombus; may be fusiform or saccular | Coronary angiography (gold standard); coronary CT angiography for size and morphology; intravascular ultrasound (IVUS) for wall characterization; echocardiography (giant aneurysms); serial imaging for surveillance | Anticoagulation with warfarin (target INR 2-3) for giant aneurysms or thrombus; antiplatelet therapy for smaller aneurysms; covered stent for suitable anatomy; surgical resection/ligation with bypass grafting for giant/symptomatic aneurysms; treat underlying cause (IVIG for Kawasaki); serial surveillance imaging every 6-12 months | Variable; small aneurysms (<5mm) have good prognosis with antiplatelet therapy; giant aneurysms carry risk of thrombosis, MI, and rupture; Kawasaki-related giant aneurysms: 50% stenotic regression but persistent risk; 5-year MACE rate 15-25% for symptomatic aneurysms | I25.41 |
| 4 | 3 | Coronary Artery Bypass Graft Stenosis | Coronary Artery Diseases | Progressive occlusive disease of bypass conduits; early (<1 month): thrombosis from technical issues; intermediate (1-12 months): intimal hyperplasia; late (>1 year): graft atherosclerosis; saphenous vein graft (SVG) more prone than internal mammary artery (IMA); risk factors: dyslipidemia, diabetes, smoking continuation | SVG patency: 80-85% at 1 year, 50-60% at 10 years; IMA patency: >95% at 10 years, >90% at 20 years; approximately 500,000+ post-CABG patients with graft disease in US | Any age post-CABG; early graft failure: within weeks of surgery; SVG atherosclerosis: 5-10 years post-surgery; late IMA disease: >15-20 years; median time to SVG intervention 8-10 years | Recurrent angina or angina equivalent; reduced exercise capacity; positive stress test; may present as ACS from acute graft thrombosis; heart failure from progressive ischemia; some patients asymptomatic with silent ischemia | Bypass graft conduits; SVG prone to intimal hyperplasia and diffuse atherosclerosis; IMA relatively protected; aorto-ostial stenosis common in SVGs; body of graft atherosclerosis is diffuse and friable | Stress imaging (preferred over exercise ECG post-CABG); coronary CT angiography for graft assessment; invasive angiography with selective graft cannulation; FFR for functional assessment; IVUS/OCT for graft characterization | Aggressive secondary prevention: high-intensity statin (target LDL <55 mg/dL); DAPT; lifestyle modification; PCI for focal SVG lesions with embolic protection device; IMA graft PCI with DES; redo CABG for extensive graft failure (higher risk, mortality 5-10%); medical therapy optimization; PCSK9 inhibitor for refractory hyperlipidemia | IMA grafts: excellent long-term patency >90% at 15 years; SVG grafts: 50% occluded by 10 years; redo CABG mortality 5-10%; PCI of SVGs has higher restenosis and MACE rates; aggressive lipid-lowering improves SVG patency; overall 5-year survival 85-90% post-CABG | I25.810 |
| 5 | 4 | Coronary Artery Disease (Chronic) | Coronary Artery Diseases | Progressive atherosclerotic plaque buildup in coronary arteries; chronic endothelial inflammation; lipid deposition; calcification over decades; risk factors: hypertension, diabetes, dyslipidemia, smoking, obesity, family history | Most common cause of death worldwide; 200 million affected globally; prevalence 7-10% in adults >40 years; US prevalence ~20.5 million (AHA 2023) | Subclinical disease begins in 20s-30s; symptomatic typically >50 years; coronary artery calcium detectable from 40s; earlier onset with familial hypercholesterolemia (heterozygous LDL >190 mg/dL) | May be asymptomatic for decades; exertional chest pain or dyspnea; reduced exercise tolerance; fatigue; silent ischemia in 25% (especially diabetics); angina equivalent symptoms in elderly | All epicardial coronary arteries; diffuse atherosclerosis with focal stenoses; plaque burden in intima and media; coronary calcification; myocardial fibrosis from chronic ischemia | Coronary artery calcium (CAC) score (Agatston); coronary CT angiography (cCAC >100 significant); stress testing modalities; invasive angiography with FFR/iFR for functional significance; lipid panel; HbA1c; hs-CRP | Lifestyle modification (Mediterranean diet, 150 min/week moderate exercise); aspirin 81mg daily; high-intensity statin (target LDL <70 mg/dL, <55 if very high risk); PCSK9 inhibitor (evolocumab 140mg q2w) if statin-insufficient; ezetimibe 10mg add-on; ACE inhibitor; revascularization for refractory symptoms or significant ischemia | Variable; 10-year ASCVD risk score guides management; annual mortality 1-3% with optimal therapy; higher with reduced EF, multivessel disease, diabetes; modern therapy improves 10-year survival to >85% | I25.10 |
| 6 | 5 | Coronary Artery Ectasia | Coronary Artery Diseases | Diffuse dilation of coronary arteries >1.5x adjacent normal segment without focal aneurysm; strongly associated with atherosclerosis (50%); connective tissue disorders; vasculitis; chronic cocaine use; enzymatic degradation of media (metalloproteinases) | Prevalence 1.2-4.9% on coronary angiography; isolated ectasia without stenosis in 10-20% of cases; more common in males (3:1 ratio); higher prevalence in Mediterranean populations | 55-70 years (atherosclerotic); younger with connective tissue disorders or vasculitis; mean age at diagnosis 60 years; incidental finding during angiography for other indications | May be asymptomatic; angina from sluggish flow and microthromboembolism; acute MI from in-situ thrombosis; positive stress test despite non-obstructive disease; atypical chest pain | Coronary arteries with diffuse dilation; RCA most commonly affected; may involve multiple vessels; sluggish flow with contrast stasis on angiography; intimal-medial thinning; loss of elastic lamina | Coronary angiography showing diffuse dilation and slow flow (Markis classification Types I-IV); TIMI frame count elevated; coronary CT angiography for luminal assessment; IVUS for wall characterization; workup for connective tissue disorders and vasculitis | Antiplatelet therapy (aspirin 81mg); anticoagulation with warfarin for severe ectasia (Type I-II) or prior thrombotic event; statin therapy; ACE inhibitor; nitrates may worsen slow flow; lifestyle modification; surveillance angiography; treat underlying cause | Similar long-term mortality to obstructive CAD; 5-year MACE rate 15-20%; risk of acute thrombotic events; prognosis worse with coexisting coronary stenosis; isolated ectasia has better outcomes; anticoagulation reduces thrombotic events | I25.89 |
| 7 | 6 | Coronary Microvascular Disease | Coronary Artery Diseases | Dysfunction of small coronary arteries and arterioles (<500 micrometers); endothelial dysfunction; impaired vasodilatory capacity; structural remodeling with medial hypertrophy; often associated with hypertension, diabetes, obesity, estrogen deficiency | Present in 50-65% of women and 30-40% of men with angina and non-obstructive coronary arteries (INOCA); estimated 3-4 million affected in US; increasingly recognized entity | More common in postmenopausal women (50-65 years); also affects younger women with risk factors; men affected but less commonly diagnosed; median age at diagnosis 55 years | Exertional angina or angina equivalent; prolonged chest pain episodes (>10 minutes); limited response to nitroglycerin; exercise intolerance; dyspnea; fatigue; microvascular angina may occur at rest; triggered by emotional stress | Coronary microcirculation (arterioles <500 micrometers); diffuse disease without focal epicardial stenosis; endothelial and smooth muscle dysfunction; structural remodeling | Coronary angiography showing non-obstructive arteries; coronary flow reserve (CFR <2.0 abnormal) measured by PET or Doppler; index of microcirculatory resistance (IMR >25); acetylcholine provocation testing for endothelial dysfunction; cardiac MRI for subendocardial ischemia | ACE inhibitor or ARB; statin therapy; beta-blocker or calcium channel blocker for symptom control; ranolazine 500-1000mg BID; low-dose aspirin; exercise training program; risk factor modification; L-arginine supplementation; nitrates may worsen symptoms; EECP (enhanced external counterpulsation) for refractory cases | Not benign as previously thought; MACE rate 2.5% per year; 5-year event rate 10-15%; reduced quality of life; hospitalization rates similar to obstructive CAD; worse prognosis with CFR <2.0 and abnormal IMR; 10-year mortality comparable to 1-vessel obstructive CAD | I25.89 |
| 8 | 7 | In-Stent Restenosis | Coronary Artery Diseases | Neointimal hyperplasia within previously stented coronary segment; smooth muscle cell proliferation and extracellular matrix deposition; rates: bare-metal stent 20-40%, first-generation DES 5-10%, current-generation DES <5%; risk factors: diabetes, small vessels, long lesions, prior restenosis | Declining with modern DES; occurs in <5% of current DES implantations; higher rates in complex lesions, bifurcations, and chronic total occlusions; remains a clinical challenge with recurrence rates 10-30% after treatment | Any age post-PCI; typically presents 3-12 months after BMS implantation; DES restenosis can occur later (6-24 months); neoatherosclerosis-driven very late restenosis (>2 years) | Recurrent angina; positive stress test after period of improvement; may present as ACS in 10-15%; exercise intolerance; dyspnea; gradual symptom recurrence months after initial PCI | Previously stented coronary artery segment; neointimal tissue within stent lumen; Mehran classification: focal (I) vs diffuse (II) vs proliferative (III) vs total occlusion (IV); neoatherosclerosis in late restenosis | Coronary angiography showing >50% diameter stenosis within stent or 5mm margins; FFR <0.80 for functional significance; IVUS/OCT to characterize mechanism (neointimal hyperplasia vs neoatherosclerosis vs stent underexpansion); stress testing for ischemia | Drug-coated balloon angioplasty (paclitaxel-coated, preferred for DES-ISR); repeat DES implantation (stent-in-stent); IVUS/OCT-guided optimization; high-pressure non-compliant balloon for underexpansion; excimer laser for resistant lesions; CABG for recurrent restenosis or multivessel disease; intravascular lithotripsy for calcified neoatherosclerosis | Target lesion revascularization rate 10-20% at 1 year after treatment; drug-coated balloon and repeat DES have similar outcomes; recurrence rate higher with each treatment; CABG provides durable solution for recurrent ISR; long-term prognosis depends on overall CAD burden | T82.855A |
| 9 | 8 | Myocardial Bridge | Coronary Artery Diseases | Congenital variant where segment of epicardial coronary artery tunnels through myocardium (normally on surface); systolic compression of bridged segment; depth >2mm and length >20mm more clinically significant; may cause ischemia from systolic compression extending into diastole | Common incidental finding; autopsy prevalence 15-85%; angiographic prevalence 0.5-16%; clinically significant in <5% of carriers; LAD bridging in >75% of cases | Congenital (present from birth); symptomatic presentation typically 40-60 years; can manifest in young athletes; earlier with additional cardiac conditions or extreme physical exertion | Often asymptomatic; exertional angina; exercise-induced ischemia; palpitations; dyspnea on exertion; rarely acute MI or sudden cardiac death (particularly in young athletes); symptoms may mimic typical CAD | Mid-LAD most common (70-98%); intramyocardial course of coronary artery; systolic compression with milking effect; depth and length determine significance; may coexist with proximal atherosclerosis due to altered shear stress | Coronary angiography showing systolic compression with milking effect; coronary CT angiography (best for anatomy, showing intramyocardial course); diastolic FFR <0.76 indicates hemodynamic significance; intravascular Doppler showing diastolic flow acceleration; exercise stress testing for ischemia | First-line: beta-blocker (metoprolol 50-200mg) to reduce heart rate and prolong diastole; calcium channel blocker (verapamil or diltiazem); avoid nitrates (worsen compression); avoid vigorous exercise if symptomatic; surgical myotomy (unroofing) for refractory symptoms; coronary bypass grafting for severe cases; stenting controversial (high restenosis risk) | Excellent for most; benign incidental finding in majority; symptomatic patients respond well to beta-blockers (>80%); rare sudden cardiac death risk in deep bridges with tachycardia; surgical unroofing provides durable symptom relief; 5-year survival >99% for uncomplicated cases | Q24.5 |
| 10 | 9 | Non-ST-Elevation Myocardial Infarction (NSTEMI) | Coronary Artery Diseases | Partial coronary artery occlusion or microembolization from plaque rupture/erosion; subendocardial ischemia with myocardial necrosis; demand ischemia (Type 2 MI) from anemia, tachycardia, hypotension | More common than STEMI; ~550,000 cases annually in US; increasing incidence due to high-sensitivity troponin assays; accounts for ~60-70% of all MIs | Older than STEMI patients; mean age 68 years; more common in women, diabetics, and elderly; Type 2 MI often in critically ill patients | Chest pain or equivalent (dyspnea, fatigue) lasting >20 minutes; may wax and wane; less severe than STEMI typically; elderly and diabetics may have atypical presentations; troponin elevation with rise/fall pattern | Partial coronary occlusion or distal microembolization; subendocardial necrosis (non-transmural); may involve multiple vessels; coronary plaque rupture with non-occlusive thrombus | Serial high-sensitivity troponin with rise/fall pattern (delta >20%); 12-lead ECG: ST depression, T-wave inversion, or normal; GRACE risk score for risk stratification; echocardiography; coronary angiography (within 24h for high-risk, 24-72h for intermediate-risk) | Dual antiplatelet therapy; anticoagulation; beta-blocker; nitroglycerin; high-intensity statin; early invasive strategy for high-risk features (GRACE >140, troponin rise, ST changes, hemodynamic instability); PCI with DES for culprit lesion; CABG if multivessel or left main disease | In-hospital mortality 3-5%; similar long-term mortality to STEMI at 6 months; 1-year mortality 7-10%; GRACE score guides prognosis; higher long-term risk due to older age and comorbidities; 5-year mortality 20-25% | I21.4 |
| 11 | 10 | Prinzmetal (Variant) Angina | Coronary Artery Diseases | Coronary artery vasospasm causing transient transmural ischemia; smooth muscle hyperreactivity; endothelial dysfunction; triggers include smoking, cocaine, cold exposure, hyperventilation, magnesium deficiency | Rare; <2% of angina cases; more common in Japanese and Korean populations; female-to-male ratio 1:5; strongly associated with smoking | Younger than typical CAD patients; 40-50 years; often without traditional cardiovascular risk factors except smoking | Recurrent episodes of severe chest pain at rest, typically between midnight and early morning; episodes last 5-15 minutes; may be accompanied by syncope or cardiac arrest from arrhythmias; ST elevation during episodes that resolves spontaneously | Epicardial coronary arteries; focal or diffuse spasm; may have underlying mild atherosclerosis at spasm sites; RCA most commonly affected; can cause MI if prolonged | ECG during episode: transient ST elevation that resolves; Holter monitoring for nocturnal ST changes; provocative testing with IV acetylcholine or ergonovine during angiography (sensitivity >90%); coronary angiography may be normal between episodes | Calcium channel blockers first-line (diltiazem 180-360mg or amlodipine 5-10mg daily); long-acting nitrates (isosorbide mononitrate 30-120mg); smoking cessation essential; avoid beta-blockers (may worsen spasm due to unopposed alpha-mediated vasoconstriction); nicorandil as adjunct; ICD if survived cardiac arrest | Good with calcium channel blocker therapy; >95% 5-year survival with treatment; risk of MI ~15% and sudden death ~10% if untreated; recurrence common if smoking continues; prognosis worse with coexisting fixed coronary stenosis | I20.1 |
| 12 | 11 | ST-Elevation Myocardial Infarction (STEMI) | Coronary Artery Diseases | Complete thrombotic occlusion of epicardial coronary artery from ruptured atherosclerotic plaque; transmural myocardial ischemia progressing to necrosis; rare causes include coronary embolism, dissection, vasospasm | ~340,000 cases annually in US; incidence 50-60 per 100,000; declining due to primary prevention and rapid reperfusion; male-to-female ratio 3:1 | Mean age 65 years for males, 72 for females; can occur in 30s-40s with familial hypercholesterolemia, cocaine use, or strong risk factors | Severe crushing substernal chest pain >20 minutes; radiation to left arm, jaw, back; unrelieved by nitroglycerin; profuse diaphoresis; nausea/vomiting; dyspnea; sense of impending doom; inferior STEMI may present with bradycardia and hypotension | Complete occlusion of epicardial coronary artery; LAD (40-50%), RCA (30-40%), LCx (15-20%); transmural myocardial necrosis; potential complications: papillary muscle rupture, VSD, free wall rupture | 12-lead ECG: ST elevation >=1mm in >=2 contiguous leads (>=2mm in V1-V3); new LBBB with ischemic symptoms; high-sensitivity troponin I/T markedly elevated; echocardiography showing regional wall motion abnormalities; coronary angiography during primary PCI | Primary PCI within 90 minutes (door-to-balloon); aspirin 325mg + P2Y12 inhibitor (ticagrelor 180mg or prasugrel 60mg); heparin bolus; GP IIb/IIIa inhibitor if needed; fibrinolysis (tenecteplase weight-based) if PCI unavailable within 120 min; beta-blocker within 24h; ACE inhibitor (ramipril 2.5-10mg); high-intensity statin; aldosterone antagonist if EF <=40% | In-hospital mortality 5-7% with primary PCI; 30-day mortality 8-10% overall; 1-year mortality 10-12%; EF <40% and Killip class >=III worsen prognosis; door-to-balloon time <90 min critical; 5-year survival ~85% with modern therapy | I21.3 |
| 13 | 12 | Spontaneous Coronary Artery Dissection (SCAD) | Coronary Artery Diseases | Non-atherosclerotic, non-traumatic separation of coronary artery wall layers; intramural hematoma compresses true lumen; associated with fibromuscular dysplasia (60-80%), pregnancy/postpartum, connective tissue disorders, hormonal factors, extreme physical/emotional stress | Accounts for 1-4% of all ACS; up to 35% of ACS in women <50 years; annual incidence estimated at 2-4 per 100,000; predominantly affects women (>90%) | Mean age 44-53 years; 90% female; peripartum SCAD: late pregnancy to 3 months postpartum; can affect younger women in 20s-30s; rare in men | Acute chest pain mimicking MI; troponin elevation; may present as STEMI or NSTEMI; cardiogenic shock in severe cases; ventricular arrhythmias; recurrent episodes in 10-30% | Any coronary artery; LAD most common (35-45%); intramural hematoma within media; intimal tear may or may not be present; often involves mid-to-distal segments; multivessel in 10-15% | Coronary angiography showing Type 1 (contrast staining), Type 2 (diffuse smooth narrowing, most common 60-75%), or Type 3 (mimics atherosclerosis); intracoronary imaging (OCT/IVUS) for equivocal cases; screening for FMD with renal/iliac angiography; genetic testing if connective tissue disorder suspected | Conservative management preferred for stable patients (spontaneous healing in 4-8 weeks); PCI high risk of propagating dissection (used only for ongoing ischemia with left main/proximal LAD involvement); CABG for failed PCI or left main; beta-blocker for shear stress reduction; avoid antiplatelet therapy beyond aspirin in conservatively managed; cardiac rehabilitation; genetic counseling; screening for FMD | Excellent acute survival >95%; in-hospital mortality 1-2%; recurrence rate 10-30% over 5-10 years; 10-year MACE rate 20-30%; pregnancy-associated SCAD has higher complication rates; avoid future pregnancy if peripartum SCAD; long-term monitoring for FMD complications | I25.42 |
| 14 | 13 | Stable Angina Pectoris | Coronary Artery Diseases | Atherosclerotic plaque causing fixed coronary stenosis >70%; endothelial dysfunction; risk factors include hypertension, dyslipidemia, diabetes, smoking | ~112 million globally (GBD 2019); prevalence 5-7% in adults >45 years in developed nations | Typically >50 years; earlier in males (45+) vs females (55+); accelerated onset with diabetes or familial hypercholesterolemia | Predictable exertional chest pressure/tightness radiating to left arm, jaw, or back; dyspnea on exertion; relieved by rest or nitroglycerin within 3-5 minutes; Levine sign; associated diaphoresis | Epicardial coronary arteries; left anterior descending (LAD) most common; atherosclerotic plaque in intima; myocardial oxygen supply-demand mismatch | Exercise stress testing (sensitivity 68%, specificity 77%); stress echocardiography; myocardial perfusion imaging (SPECT/PET); coronary CT angiography (sensitivity >95%); invasive coronary angiography gold standard; fractional flow reserve (FFR <0.80 significant) | Aspirin 81mg daily; high-intensity statin (atorvastatin 40-80mg or rosuvastatin 20-40mg); beta-blocker (metoprolol succinate 25-200mg); sublingual nitroglycerin PRN; calcium channel blocker (amlodipine 5-10mg) if beta-blocker contraindicated; ranolazine 500-1000mg BID for refractory symptoms; PCI with DES for significant stenosis; CABG for left main or 3-vessel disease | Good with optimal medical therapy; annual mortality 1-3% with stable disease; 5-year survival >90% with revascularization when indicated; reduced survival with EF <40% or left main disease | I20.8 |
| 15 | 14 | Unstable Angina | Coronary Artery Diseases | Acute plaque rupture or erosion with non-occlusive thrombus formation; plaque vulnerability from thin fibrous cap and large lipid core; vasospasm; progressive luminal narrowing | Part of ACS spectrum; ~780,000 ACS events annually in US; unstable angina declining due to high-sensitivity troponin reclassifying many as NSTEMI | 50-70 years; earlier in males; increasing incidence with age; accelerated in diabetes, CKD, and prior CAD | New-onset or crescendo angina; rest angina lasting >20 minutes; chest pain not fully relieved by nitroglycerin; pain at lower thresholds than usual; associated dyspnea, diaphoresis, nausea; no troponin elevation | Coronary arteries with vulnerable atherosclerotic plaques; partial thrombotic occlusion; subendocardial ischemia without necrosis | Serial high-sensitivity troponin (must be negative); 12-lead ECG showing ST depression or T-wave inversion; TIMI or GRACE risk score; coronary angiography for risk stratification; stress testing if low-intermediate risk | Dual antiplatelet therapy (aspirin 325mg loading + clopidogrel 300-600mg or ticagrelor 180mg loading); anticoagulation with enoxaparin 1mg/kg BID or heparin drip; beta-blocker (metoprolol 25-50mg); nitroglycerin IV; high-intensity statin; early invasive strategy (angiography within 24-72h) for high-risk features; PCI with DES as indicated | Good with early invasive strategy; 30-day mortality <2%; 1-year MACE rate 10-15%; higher risk with positive troponin trend, ST changes, hemodynamic instability, or GRACE score >140 | I20.0 |
| 16 | ▸ HEART FAILURE SYNDROMES (12 disorders) | |||||||||||
| 17 | 15 | Acute Decompensated Heart Failure | Heart Failure Syndromes | Rapid worsening of HF signs and symptoms requiring urgent treatment; triggers: medication non-adherence (most common), dietary indiscretion, acute ischemia, arrhythmia (new AF), infection, anemia, renal dysfunction, uncontrolled hypertension, pulmonary embolism | ~1 million HF hospitalizations annually in US; 30-day readmission rate 20-25%; accounts for >6 million hospital days per year; most costly diagnosis in Medicare patients | Mean age 72-75 years for hospitalization; increasing with age; can occur at any age with underlying cardiomyopathy; recurrent episodes common (50% readmit within 6 months) | Acute dyspnea at rest; inability to lie flat; severe peripheral edema; weight gain (>2kg in 48 hours); pulmonary rales; jugular venous distension; S3 gallop; cool extremities (low-output) or warm and edematous (wet-warm profile); hepatic congestion; altered mental status if cardiogenic shock | Overwhelmed cardiac compensation; elevated filling pressures; pulmonary congestion; systemic venous congestion; may have reduced or preserved EF; hemodynamic profiles: wet-warm (most common, 67%), wet-cold (28%), dry-warm, dry-cold | BNP >400 pg/mL or NT-proBNP >900 pg/mL (age-adjusted); chest X-ray (pulmonary edema, pleural effusions); echocardiography (EF, valvular function); troponin (rule out ACS); basic metabolic panel (renal function, electrolytes); lung ultrasound (B-lines); invasive hemodynamics with PA catheter if uncertain | IV loop diuretic (furosemide 20-80mg IV bolus, double home dose); vasodilators (nitroglycerin IV for hypertensive presentations); inotropes (dobutamine 2-20 mcg/kg/min or milrinone 0.375-0.75 mcg/kg/min) for cardiogenic shock; oxygen/NIV for respiratory distress; restrict sodium <2g/day and fluids <1.5L/day; identify and treat trigger; uptitrate GDMT before discharge; early follow-up within 7 days | In-hospital mortality 4-7%; 30-day mortality 10-12%; 1-year mortality 25-35% post-hospitalization; each hospitalization worsens long-term prognosis; readmission rate 50% at 6 months; predictors of poor outcome: hypotension, elevated BUN/creatinine, hyponatremia, elevated troponin | I50.21 |
| 18 | 16 | Biventricular Heart Failure | Heart Failure Syndromes | Combined left and right ventricular dysfunction; most commonly from progression of left heart failure causing secondary pulmonary hypertension and RV failure; ischemic cardiomyopathy; dilated cardiomyopathy; severe valvular disease; advanced cardiac amyloidosis; chronic volume overload | Present in 20-30% of advanced HF patients; common in end-stage cardiomyopathy; higher prevalence in hospitalized HF patients; associated with highest mortality among HF subtypes | 60-75 years; more common in advanced stages of any cardiomyopathy; earlier in aggressive forms (cardiac amyloidosis, Chagas disease, advanced ischemic cardiomyopathy) | Combined symptoms of left and right HF; severe dyspnea at rest; anasarca; ascites; jugular venous distension; bibasilar rales; hepatomegaly; low cardiac output symptoms (fatigue, altered mentation, cool extremities); refractory to diuretics; Cheyne-Stokes respiration | Both ventricles dilated and dysfunctional; severe diastolic dysfunction; moderate-severe mitral and tricuspid regurgitation; pulmonary hypertension; systemic venous congestion; reduced cardiac output; multi-organ hypoperfusion | Echocardiography showing biventricular dilation and dysfunction; elevated BNP/NT-proBNP (often >5000 pg/mL); invasive hemodynamics: elevated PCWP and RAP, reduced cardiac index (<2.2 L/min/m2), elevated PVR; cardiac MRI; peak VO2 <14 mL/kg/min indicates advanced HF | Aggressive GDMT; IV diuretics and vasodilators; inotropic support (milrinone preferred for RV component); biventricular pacing (CRT) if LBBB + QRS >=150ms; ICD for sudden death prevention; consideration for advanced therapies: LVAD as bridge or destination therapy; heart transplant evaluation (definitive treatment); palliative care discussion if not transplant candidate | Poor; 1-year mortality 30-50%; median survival 2-4 years without advanced therapy; CRT improves survival by 20-30% in appropriate candidates; LVAD improves 2-year survival to 50-70%; heart transplant: 1-year survival 85-90%, median 12-13 years; RV failure post-LVAD worsens outcomes | I50.82 |
| 19 | 17 | Cardiac Amyloidosis (ATTR) | Heart Failure Syndromes | Extracellular deposition of misfolded transthyretin (TTR) protein in myocardium; wild-type ATTR (ATTRwt, senile) from age-related TTR instability; hereditary ATTR (ATTRv) from TTR gene mutations (V122I in 3-4% of African Americans, T60A most common globally); causes restrictive cardiomyopathy with progressive diastolic and systolic dysfunction | Increasingly recognized; ATTRwt in 13-25% of HFpEF patients >60 years; found in 17% of TAVR patients; hereditary ATTR: V122I allele in 3-4% of African Americans (carrier frequency); estimated 300,000-500,000 affected in US; dramatically underdiagnosed | ATTRwt: typically >65-70 years (almost exclusively male at diagnosis); ATTRv V122I: 60-80 years; ATTRv T60A: 50-70 years; some mutations present in 30s-40s; bilateral carpal tunnel syndrome often precedes cardiac symptoms by 5-10 years | Progressive HFpEF symptoms; exertional dyspnea; exercise intolerance; peripheral edema; bilateral carpal tunnel syndrome (preceding cardiac symptoms); lumbar spinal stenosis; atrial fibrillation; conduction abnormalities (may need pacemaker); orthostatic hypotension (autonomic neuropathy in ATTRv); low-voltage QRS paradoxically with thick ventricles | Biventricular myocardial thickening (non-dilated, restrictive pattern); amyloid fibrils in extracellular space between myocytes; atrial enlargement; valvular thickening; granular sparkling on echo; conduction system infiltration; diastolic dysfunction progressing to restrictive physiology | Echocardiography: increased wall thickness (>12mm), diastolic dysfunction, apical sparing pattern on strain (cherry-on-top); technetium pyrophosphate (Tc-PYP) scintigraphy: Grade 2-3 uptake diagnostic for ATTR without biopsy (if AL excluded); cardiac MRI: diffuse subendocardial or transmural LGE, elevated native T1, elevated ECV (>0.40); serum free light chains and immunofixation (to exclude AL); TTR gene sequencing; endomyocardial biopsy with Congo red staining (apple-green birefringence) and mass spectrometry | Tafamidis 80mg daily (TTR stabilizer, ATTR-ACT trial: 30% reduction in mortality + hospitalization); diflunisal 250mg BID (off-label TTR stabilizer); acoramidis (investigational, ATTRibute-CM trial positive); for ATTRv: patisiran or inotersen (RNA silencers); diuretics (carefully, preload-dependent); pacemaker for conduction disease; avoid digoxin, CCBs, beta-blockers in advanced disease; heart transplant for selected young ATTRv patients; liver transplant for ATTRv (removes mutant TTR source) | ATTRwt: median survival 3.5-5 years from diagnosis; ATTRv V122I: median survival 2.5-4 years; tafamidis improves survival by 30%; NYHA class III/IV: median survival 18-24 months; earlier diagnosis and treatment improving outcomes; 5-year survival improving from 20% to 40-50% with tafamidis; cardiac biomarkers (troponin, NT-proBNP) are strongest prognostic markers | E85.4 |
| 20 | 18 | Cardiac Cachexia | Heart Failure Syndromes | Involuntary non-edematous weight loss >5% over 6-12 months in chronic HF; multifactorial: neurohormonal activation (elevated TNF-alpha, IL-6), anorexia from hepatic/splanchnic congestion, impaired intestinal absorption, increased resting energy expenditure, skeletal muscle catabolism, insulin resistance | Present in 10-15% of chronic HF patients; more common in advanced HF (NYHA III-IV); prevalence increases with disease duration; marker of severely advanced disease; under-recognized and under-treated | Advanced HF population; typically 60-80 years; develops over months to years of chronic HF; more common in HFrEF than HFpEF; associated with chronic infections and malignancy in HF context | Unintentional weight loss; muscle wasting (sarcopenia); fatigue and weakness; anorexia; early satiety; temporal and extremity muscle wasting; reduced handgrip strength; poor functional capacity; depression; impaired immunity; skin changes | Systemic process affecting skeletal muscle, adipose tissue, and bone; myocardial muscle loss; diaphragmatic weakness; GI tract congestion with malabsorption; hormonal imbalance (low testosterone, GH resistance, elevated cortisol) | Clinical assessment: weight loss >5% in 6 months or BMI <20 with weight loss; DEXA for body composition; bioelectrical impedance analysis; handgrip dynamometry; serum albumin and prealbumin; inflammatory markers (CRP, IL-6, TNF-alpha); 6-minute walk test | Optimize HF therapy (GDMT); nutritional support (high calorie, high protein diet; small frequent meals); exercise training (resistance and aerobic); appetite stimulants (megestrol, limited evidence); omega-3 fatty acids; testosterone replacement in hypogonadal males; consider ghrelin receptor agonists (investigational); ACEi may help preserve muscle; treat depression; palliative care referral | Very poor; independent predictor of mortality; 50% 18-month mortality once established; significantly worse than non-cachectic HF patients; weight loss >6% has HR 2.1 for death; often indicates end-stage HF; quality of life severely impaired; may improve with heart transplant or LVAD | R64 |
| 21 | 19 | Cardiorenal Syndrome | Heart Failure Syndromes | Bidirectional dysfunction between heart and kidneys; Type 1: acute HF causing AKI; Type 2: chronic HF causing progressive CKD; Type 3: AKI causing acute cardiac dysfunction; Type 4: CKD causing chronic cardiac disease; Type 5: systemic conditions (sepsis, amyloidosis) causing both; venous congestion, reduced renal perfusion, neurohormonal activation | CKD present in 40-50% of HF patients; AKI occurs in 25-30% of acute HF hospitalizations; worsening renal function during HF hospitalization in 20-30%; Type 2 most common | 60-80 years; age-related decline in both cardiac and renal function; earlier in diabetic nephropathy; prevalence increases with severity of HF or CKD | Combination of HF and renal symptoms; volume overload refractory to diuretics (diuretic resistance); oliguria; worsening creatinine; electrolyte imbalances; fatigue; anorexia; peripheral edema; dyspnea; anemia; uremia in advanced cases | Heart-kidney axis; renal venous congestion (elevated CVP >12 mmHg reduces GFR); reduced renal arterial perfusion; RAAS and sympathetic overactivation; inflammation and oxidative stress; shared risk factors (diabetes, hypertension, atherosclerosis) | Serial creatinine, BUN, cystatin C; urine sodium and FENA; BNP/NT-proBNP; echocardiography; renal ultrasound with Doppler; invasive hemodynamics (CVP, PCWP, cardiac output); renal resistive index; biomarkers: NGAL, KIM-1 for early AKI detection | Diuretic optimization (loop diuretic dose escalation, combination with thiazide for sequential nephron blockade); IV diuretics for acute decompensation; SGLT2 inhibitor (renal and cardiac protection, DAPA-CKD and EMPA-KIDNEY trials); ARNI (sacubitril-valsartan); finerenone for diabetic CKD; ultrafiltration for diuretic-resistant congestion; renal replacement therapy if indicated; avoid nephrotoxins; careful contrast use | Poor; coexisting HF and CKD doubles mortality; 1-year mortality 30-40% after cardiorenal hospitalization; worsening renal function during HF admission increases mortality by 50%; GFR <30 mL/min in HF patients: 3-year mortality >60%; SGLT2 inhibitors slow renal decline by 30-40% | I13.2 |
| 22 | 20 | Heart Failure with Mildly Reduced EF (HFmrEF) | Heart Failure Syndromes | EF 41-49%; intermediate phenotype between HFrEF and HFpEF; may represent recovering HFrEF or early declining HFpEF; shares features of both; similar risk factor profile to HFpEF but higher rate of coronary artery disease | Accounts for 10-25% of HF cases; increasingly recognized as distinct entity since 2016 ESC guidelines; prevalence estimated 1-2 million in US | Similar to HFrEF and HFpEF; mean age 65-70 years; male predominance (55-60%); higher rate of ischemic etiology compared to HFpEF | Similar to HFrEF: exertional dyspnea, exercise intolerance, peripheral edema, fatigue; clinical profile intermediate between HFrEF and HFpEF; may transition to either phenotype over time | Left ventricle with mildly impaired systolic function; may have diastolic dysfunction; variable remodeling pattern; coronary artery disease common; intermediate neurohormonal activation | Echocardiography: EF 41-49%; BNP/NT-proBNP elevated; same workup as other HF subtypes; coronary assessment; cardiac MRI; serial echocardiography to track EF trajectory | Evidence extrapolated from HFrEF trials (subgroup analyses suggest benefit); SGLT2 inhibitor (dapagliflozin/empagliflozin, DELIVER trial included EF >40%); ACEi/ARB/ARNI (PARAGON-HF borderline benefit in EF <57%); beta-blocker; MRA; diuretics for congestion; treat underlying etiology; reassess EF regularly as may shift to HFrEF or recover | Intermediate prognosis between HFrEF and HFpEF; annual mortality 5-10%; 5-year mortality 30-40%; may improve to normal EF (recovered HF) with optimal therapy in 30-40%; those transitioning to HFrEF have worse outcomes; SGLT2 inhibitors show consistent benefit across EF spectrum | I50.40 |
| 23 | 21 | Heart Failure with Preserved Ejection Fraction (HFpEF) | Heart Failure Syndromes | Diastolic dysfunction with EF >=50%; impaired ventricular relaxation and increased stiffness; multifactorial: obesity, hypertension, diabetes, atrial fibrillation, aging, chronic kidney disease; systemic microvascular inflammation hypothesis; coronary microvascular dysfunction | Accounts for ~50% of all HF cases; increasing prevalence; estimated 3-4 million in US; more common in elderly women; represents the growing epidemic of HF | Typically >65 years; female predominance (60-65%); strong association with metabolic syndrome; median age at diagnosis 70-75 years; rarely diagnosed before 50 | Exertional dyspnea (most common); exercise intolerance; fatigue; peripheral edema; orthopnea less prominent than HFrEF; abdominal bloating; may have preserved resting function but impaired exercise hemodynamics | Left ventricle with normal or near-normal systolic function but impaired relaxation; concentric remodeling/hypertrophy; left atrial enlargement; elevated filling pressures; increased ventricular-arterial stiffness; extracellular matrix fibrosis | Echocardiography: EF >=50% with diastolic dysfunction (E/e' >=14, e' septal <7 cm/s); elevated BNP/NT-proBNP (may be lower than HFrEF); H2FPEF score (>=6 points diagnostic); HFA-PEFF algorithm; exercise right heart catheterization (PCWP >=25 mmHg with exercise) gold standard; cardiac MRI for fibrosis (T1 mapping) | SGLT2 inhibitor (empagliflozin 10mg, EMPEROR-Preserved trial showed 21% reduction in HF hospitalization); diuretics for congestion; treat comorbidities aggressively (hypertension, AF, obesity, diabetes); weight loss (if BMI >30); exercise training (improves peak VO2); GLP-1 receptor agonist (semaglutide, STEP-HFpEF trial showed symptom improvement); MRA (spironolactone, borderline benefit); no proven mortality-reducing therapy | Annual mortality 5-8%; lower than HFrEF short-term but similar long-term; 5-year mortality 35-45%; frequent hospitalizations (50% readmit within 6 months); quality of life significantly impaired; cardiovascular death accounts for 50-60% of deaths; no therapy yet proven to reduce mortality | I50.30 |
| 24 | 22 | Heart Failure with Reduced Ejection Fraction (HFrEF) | Heart Failure Syndromes | Left ventricular systolic dysfunction with EF <=40%; causes: ischemic cardiomyopathy (most common, 60-70%), idiopathic dilated cardiomyopathy, valvular disease, hypertension, myocarditis, toxins (alcohol, chemotherapy), tachycardia-mediated | ~6.7 million adults in US with HF (AHA 2023); HFrEF accounts for ~50% of HF cases; lifetime risk 20-25%; prevalence increasing with aging population; 1 million hospitalizations annually | Increasing with age; mean age at diagnosis 65-75 years; earlier onset with ischemic etiology in males; prevalence doubles each decade after 45 years | Exertional dyspnea; orthopnea; paroxysmal nocturnal dyspnea; peripheral edema; fatigue; exercise intolerance; weight gain from fluid retention; elevated JVP; S3 gallop; pulmonary rales; hepatomegaly; Cheyne-Stokes respiration | Left ventricle with reduced contractility; ventricular dilation and eccentric remodeling; neurohormonal activation (RAAS, sympathetic); elevated natriuretic peptides; secondary mitral regurgitation; biventricular dysfunction in advanced disease | Echocardiography (LVEF <=40%); BNP >100 pg/mL or NT-proBNP >300 pg/mL; cardiac MRI for etiology (LGE pattern); coronary angiography to assess ischemic etiology; chest X-ray (cardiomegaly, pulmonary congestion); ECG; stress testing; endomyocardial biopsy if infiltrative disease suspected | GDMT quadruple therapy: ACEi/ARB/ARNI (sacubitril-valsartan 97/103mg BID), beta-blocker (carvedilol 25mg BID or metoprolol succinate 200mg), MRA (spironolactone 25-50mg or eplerenone 50mg), SGLT2 inhibitor (dapagliflozin 10mg or empagliflozin 10mg); loop diuretic (furosemide) for congestion; hydralazine-nitrate in Black patients; ICD for EF <=35%; CRT if EF <=35% + LBBB + QRS >=150ms; LVAD or heart transplant for advanced HF | 5-year mortality 50-75% without treatment; GDMT reduces mortality by 60-70%; 1-year mortality 20-25% after HF hospitalization; NYHA class IV: 50% 1-year mortality; ICD reduces sudden death by 23%; CRT improves symptoms and survival; heart transplant: median survival 12-13 years | I50.20 |
| 25 | 23 | High-Output Heart Failure | Heart Failure Syndromes | Heart failure despite elevated cardiac output (>8 L/min or cardiac index >4 L/min/m2); systemic vasodilation or AV shunting increases cardiac demand beyond capacity; causes: severe anemia, thyrotoxicosis, obesity, Paget disease, AV fistula (dialysis or traumatic), beriberi (thiamine deficiency), liver cirrhosis, sepsis, pregnancy | Rare; accounts for <1% of all HF cases; more common in sub-Saharan Africa (beriberi, malnutrition); increasing recognition in morbid obesity and chronic hemodialysis patients with AV fistulas | Variable depending on cause; thyrotoxicosis: 30-60 years; dialysis AV fistula: any age on dialysis; obesity: 40-60 years; Paget disease: >50 years; beriberi: any age (alcoholics, malnutrition) | HF symptoms despite bounding pulses and warm extremities; wide pulse pressure; tachycardia; systolic flow murmurs; peripheral vasodilation; may have signs of underlying cause (goiter, AV fistula thrill, pallor from anemia); exercise intolerance; dyspnea | Ventricles may be normal or dilated with preserved systolic function initially; increased preload from high venous return; biventricular dilation with prolonged high-output state; eventual systolic dysfunction; volume overload of all cardiac chambers | Echocardiography: elevated cardiac output on Doppler; may show dilated chambers with preserved or mildly reduced EF; invasive hemodynamics: high CO, low SVR, elevated mixed venous oxygen saturation >75%; identify underlying cause: TSH, hemoglobin, thiamine level, liver function, AV fistula flow assessment | Treat underlying cause (essential): correct anemia (transfusion, EPO), treat thyrotoxicosis (methimazole, radioactive iodine), AV fistula banding/ligation if flow >2L/min, thiamine replacement (100mg IV then 100mg oral daily for beriberi), weight loss for obesity; diuretics for congestion; digoxin may help; beta-blockers cautiously; avoid afterload reduction (already vasodilated) | Good if underlying cause is correctable; beriberi responds dramatically to thiamine; thyrotoxic HF resolves with thyroid control; AV fistula banding improves symptoms; refractory if cause cannot be addressed; mortality depends on underlying condition; prolonged high-output state leads to irreversible LV dysfunction | I50.83 |
- Full dataset access
- Excel format
- Instant download