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Basic - Cardiac Profile

Heart

15 parameters

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Report in 8Hrs

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At Home

fastingrequire

Fasting Required

Details

Comprehensive profile (lipids, enzymes, troponins, hs-CRP).

₹999₹1,469

32% OFF

Parameters

  • List of Tests
    • hs-CRP
    • Lipoprotein (A)
    • Uric Acid
    • Homocysteine
    • Apoliprotein A1
    • Apoliprotein B
    • Apo B/A1
    • Cholesterol/HDL
    • LDL/HDL
    • Non-HDL
    • VLDL
    • Total Cholesterol
    • Triglycerides
    • HDL
    • LDL

Basic - Cardiac Profile

  • Why is it done?
    • This comprehensive panel assesses cardiovascular risk by evaluating lipid metabolism, inflammation markers, and metabolic factors that contribute to heart disease and atherosclerosis
    • hs-CRP (high-sensitivity C-Reactive Protein) measures inflammation in blood vessels, a key predictor of cardiovascular events and atherosclerotic plaque rupture
    • Lipoprotein (A) identifies genetic predisposition to elevated cardiovascular risk independent of cholesterol levels, particularly important for familial hypercholesterolemia screening
    • Uric Acid evaluates metabolic status and screens for gout risk; elevated levels correlate with hypertension, metabolic syndrome, and cardiovascular disease
    • Homocysteine detects hyperhomocysteinemia, an independent risk factor for thrombotic events, coronary artery disease, and peripheral vascular disease
    • Apolipoprotein A1 and B measurements provide superior risk stratification by directly quantifying HDL and LDL particle numbers, more predictive than traditional cholesterol ratios
    • Lipid Profile components (Total Cholesterol, HDL, LDL, Triglycerides, VLDL, Non-HDL) form the foundation of cardiovascular risk assessment and guide preventive therapy decisions
    • Recommended for initial cardiac risk stratification, routine health screening in adults over 40, monitoring patients on lipid-lowering therapy, and evaluating those with family history of premature coronary artery disease
    • All individual tests work synergistically to provide comprehensive cardiovascular risk profiling, identifying both traditional and emerging risk factors for personalized prevention strategies
  • Normal Range
    • hs-CRP: Less than 1.0 mg/L (optimal cardiovascular risk), 1.0-3.0 mg/L (intermediate risk), Greater than 3.0 mg/L (high cardiovascular risk)
    • Lipoprotein (A): Less than 30 mg/dL (optimal), 30-50 mg/dL (borderline elevated), Greater than 50 mg/dL (elevated risk); levels genetically determined and do not typically change with lifestyle
    • Uric Acid: Males 3.5-7.2 mg/dL, Females 2.6-6.0 mg/dL; higher values increase gout and cardiovascular risk
    • Homocysteine: Less than 10 μmol/L (normal), 10-15 μmol/L (intermediate), Greater than 15 μmol/L (elevated); higher levels represent thrombotic risk
    • Apolipoprotein A1: Males 94-178 mg/dL, Females 101-199 mg/dL; higher levels associated with better cardiovascular protection
    • Apolipoprotein B: Males 52-109 mg/dL, Females 42-119 mg/dL; reflects total atherogenic particle burden
    • Apo B/A1 Ratio: Optimal less than 0.6; ratio greater than 0.9 indicates higher cardiovascular risk
    • Total Cholesterol: Less than 200 mg/dL (desirable), 200-239 mg/dL (borderline high), Greater than 240 mg/dL (high)
    • HDL Cholesterol: Greater than 60 mg/dL (protective), 40-59 mg/dL (normal, suboptimal in males), Less than 40 mg/dL in males and less than 50 mg/dL in females (low risk factor)
    • LDL Cholesterol: Less than 100 mg/dL (optimal), 100-129 mg/dL (near optimal), 130-159 mg/dL (borderline high), 160-189 mg/dL (high), Greater than 190 mg/dL (very high)
    • Triglycerides: Less than 150 mg/dL (normal), 150-199 mg/dL (borderline high), 200-499 mg/dL (high), Greater than 500 mg/dL (very high with severe pancreatitis risk)
    • VLDL: 2-30 mg/dL; calculated by dividing triglycerides by 5, elevated levels reflect increased triglyceride-rich particles
    • Non-HDL Cholesterol: Total Cholesterol minus HDL; less than 130 mg/dL is optimal, reflects all atherogenic particles
    • Cholesterol/HDL Ratio: Less than 5.0 is desirable (men), less than 4.5 is desirable (women)
    • LDL/HDL Ratio: Less than 3.0 is optimal, less than 5.0 is acceptable, greater than 5.0 indicates elevated cardiovascular risk
  • Interpretation
    • hs-CRP Elevated: Indicates vascular inflammation and increased atherosclerosis risk; levels fluctuate with acute illness and infection; chronic elevation suggests systemic inflammation and warrants aggressive cardiovascular risk reduction
    • Lipoprotein (A) Elevated: Indicates genetic predisposition to thrombosis and atherosclerosis; remains elevated despite lifestyle changes; strongly associated with myocardial infarction and stroke risk; warrants consideration of aggressive preventive therapy
    • Uric Acid Elevated: Indicates hyperuricemia, associated with gout, chronic kidney disease, metabolic syndrome, hypertension, and increased cardiovascular mortality; may reflect impaired renal clearance or dietary overload
    • Uric Acid Decreased: Rare; may indicate xanthine oxidase deficiency or result of allopurinol therapy; generally not clinically significant
    • Homocysteine Elevated: Independent predictor of vascular thrombosis; associated with increased risk of myocardial infarction, stroke, and deep vein thrombosis; may result from B vitamin deficiency, genetic polymorphisms, or chronic kidney disease
    • Apolipoprotein A1 Decreased: Associated with reduced HDL-mediated reverse cholesterol transport; indicates loss of cardioprotection and increased atherosclerosis risk
    • Apolipoprotein B Elevated: Indicates increased number of atherogenic particles (LDL, VLDL); more predictive of cardiovascular risk than LDL-cholesterol alone; warrants intensive lipid-lowering therapy
    • Apo B/A1 Ratio Elevated: Superior predictor of cardiovascular risk compared to traditional lipid ratios; reflects imbalance between atherogenic and protective particle populations
    • Total Cholesterol Elevated: Associated with increased atherosclerosis and coronary artery disease risk; requires evaluation of HDL and LDL components for appropriate risk stratification
    • HDL Cholesterol Low: Major risk factor for atherosclerotic cardiovascular disease; associated with metabolic dysfunction, obesity, sedentary lifestyle, and smoking; improvement through exercise and smoking cessation is protective
    • HDL Cholesterol High: Protective against atherosclerotic disease; facilitates reverse cholesterol transport and has anti-inflammatory properties; associated with favorable cardiovascular outcomes
    • LDL Cholesterol Elevated: Primary driver of atherosclerosis; directly correlates with coronary plaque burden; lower levels achieved through statin therapy significantly reduce cardiovascular event risk
    • Triglycerides Elevated: Associated with metabolic dysfunction, increased small-dense LDL particles, reduced HDL, and coronary artery disease risk; very high levels (>500 mg/dL) increase acute pancreatitis risk
    • VLDL Elevated: Reflects increased triglyceride-rich lipoprotein particles; particularly atherogenic when small and dense; associated with metabolic syndrome and insulin resistance
    • Non-HDL Cholesterol Elevated: Captures all atherogenic particles; more comprehensive risk assessment than LDL alone; elevated levels warrant intensified lipid management
    • Lipid Ratios (Cholesterol/HDL and LDL/HDL): Higher ratios indicate greater cardiovascular risk; lower ratios reflect better cholesterol quality and more protective lipid profiles; useful for monitoring therapy response
    • Factors Affecting Results: Recent acute illness or infection artificially elevates hs-CRP; Lipoprotein(A) genetically determined and stable; fasting status affects triglycerides and VLDL accuracy; medications (statins, fibrates, niacin) alter lipid values; pregnancy and hormonal therapy affect lipid panel
    • False Positive Causes: hs-CRP may be elevated from arthritis, infection, or inflammation unrelated to cardiovascular disease; high Lipoprotein(A) is genetic and not modifiable; medication effects must be considered when interpreting all panel components
  • Associated Organs
    • Heart and Coronary Arteries: All tests in this panel primarily evaluate risk for atherosclerotic coronary artery disease, myocardial infarction, and heart failure; elevated inflammatory markers and lipid abnormalities directly predict coronary events
    • Blood Vessels and Endothelium: Lipid profile components and inflammatory markers assess vascular endothelial dysfunction and atherosclerotic plaque formation throughout the circulatory system
    • Brain: Homocysteine, lipid abnormalities, and inflammatory markers predict stroke risk and cerebrovascular disease; elevated Lipoprotein(A) increases thrombotic stroke risk
    • Peripheral Arteries: Elevated homocysteine, lipids, and inflammation markers are risk factors for peripheral arterial disease and claudication
    • Kidneys: Uric acid levels reflect renal function and glomerular filtration rate; elevated uric acid may indicate chronic kidney disease; hyperuricemia can cause diabetic nephropathy
    • Liver: Primary site of lipoprotein and cholesterol synthesis; liver function abnormalities affect all lipid profile components; hepatic lipase influences HDL and triglyceride metabolism
    • Pancreas: Severe hypertriglyceridemia (>500 mg/dL) significantly increases acute pancreatitis risk; triglyceride levels directly correlate with pancreatic inflammation potential
    • Vascular System: hs-CRP measures systemic vascular inflammation and endothelial activation; elevated levels predict atherosclerotic burden in coronary and peripheral vessels
    • Coagulation System: Elevated Lipoprotein(A) and homocysteine promote thrombosis; increased inflammatory markers enhance prothrombotic state and plaque destabilization
    • Associated Conditions: Atherosclerotic cardiovascular disease, familial hypercholesterolemia, metabolic syndrome, type 2 diabetes mellitus, chronic kidney disease, gout, acute coronary syndrome, stroke, peripheral arterial disease
    • Potential Complications: Myocardial infarction, unstable angina, stroke, transient ischemic attack, peripheral vascular occlusion, thrombotic events, acute pancreatitis (severe hypertriglyceridemia), sudden cardiac death
  • Follow-up Tests
    • Elevated hs-CRP: Repeat testing to confirm persistent inflammation; consider high-sensitivity testing for risk stratification; referral for inflammation workup if significantly elevated; consider advanced imaging (coronary calcium score or carotid ultrasound)
    • Elevated Lipoprotein (A): Genetic counseling recommended; screening of first-degree relatives; serial monitoring every 5 years; consideration of enhanced lipid-lowering therapy; evaluate for familial hypercholesterolemia
    • Elevated Uric Acid: Comprehensive metabolic panel to assess kidney function and glucose metabolism; urine uric acid and creatinine clearance if gout suspected; renal ultrasound if chronic kidney disease present; evaluation for secondary causes (malignancy, thiazide use)
    • Elevated Homocysteine: Vitamin B12, folate, and pyridoxal-5-phosphate levels to identify deficiency; assessment of renal function (creatinine and eGFR); genetic testing for MTHFR polymorphisms; consider thrombophilia workup
    • Abnormal Apolipoprotein Levels: Advanced lipid fractionation and lipoprotein particle number analysis (NMR or ion mobility); repeat testing 2-4 weeks after statin initiation to assess therapy response; extended lipid panels including small dense LDL
    • Elevated Total Cholesterol: Repeat lipid panel after therapeutic intervention; evaluate each component (HDL, LDL, triglycerides) separately for targeted treatment; consider genetic testing if very elevated (>300 mg/dL)
    • Low HDL Cholesterol: Lifestyle counseling regarding exercise and smoking cessation; reassess thyroid function and metabolic parameters; consider niacin, fibrate, or CETP inhibitor therapy if persistently low; repeat testing after 3-6 months
    • Elevated LDL Cholesterol: Initiate or intensify statin therapy; repeat lipid panel 4-8 weeks after medication change; consider advanced lipid testing (particle size, LDL subfractions); assess for secondary causes (hypothyroidism, nephrotic syndrome, cirrhosis)
    • Elevated Triglycerides: Repeat fasting lipid panel to confirm findings; assess glucose metabolism (fasting glucose, HbA1c); screen for metabolic syndrome and insulin resistance; if severely elevated (>500 mg/dL), evaluate for familial hypertriglyceridemia and assess pancreatitis risk
    • Elevated VLDL: Measure triglycerides directly; assess metabolic syndrome parameters including fasting glucose and blood pressure; evaluate dietary habits and alcohol consumption
    • Elevated Non-HDL Cholesterol: Therapeutic lifestyle changes and pharmacologic intervention targeting all atherogenic particles; repeat lipid panel 4-8 weeks after therapy initiation; assess for metabolic dysfunction
    • Unfavorable Lipid Ratios: Address individual components (increase HDL, decrease LDL); repeat testing every 3-6 months during therapeutic intervention; if abnormal persist, consider combination therapy or advanced lipid management strategies
    • General Follow-up Recommendations: Repeat full cardiac profile annually for risk assessment; more frequent monitoring (every 4-8 weeks) after initiating or changing lipid-lowering therapy; cardiovascular risk assessment tools (Framingham, ASCVD risk score); consider non-invasive cardiac imaging if indicated
    • Complementary Tests: Lipoprotein fractionation for particle characterization; oxidized LDL for advanced atherosclerosis assessment; blood pressure monitoring; fasting glucose and HbA1c for diabetes screening; thyroid function tests; renal function assessment; electrocardiogram and stress testing for symptomatic patients
  • Fasting Required?
    • Yes - 9-12 hours fasting is required for accurate results of this test package
    • Fasting Duration: Optimal fasting period is 9-12 hours; patient should not consume food or beverages except water after 9 PM the evening before morning testing
    • Critical for Accurate Results: Triglyceride and VLDL levels are particularly sensitive to fasting status; non-fasting triglycerides may be significantly elevated and overestimate cardiovascular risk
    • LDL Cholesterol Calculation: Calculation requires fasting state to ensure accurate triglyceride measurement for precise LDL determination using Friedewald equation
    • Water Intake: Water consumption is permitted and encouraged during fasting period to maintain hydration
    • Medications to Avoid Before Testing: Do not take lipid-lowering medications (statins, fibrates, niacin) the morning of testing; discuss with physician if these medications should be temporarily held (typically not recommended - continue as prescribed unless otherwise directed)
    • Medications to Continue: Regular cardiovascular and chronic disease medications should be continued unless physician specifically instructs otherwise
    • Dietary Restrictions Before Testing: Avoid all food, including breakfast; avoid caffeine and alcoholic beverages; avoid chewing gum containing sugar
    • Alcohol Consumption: Avoid alcohol for 24 hours before testing as it significantly affects triglyceride levels and lipid panel accuracy
    • Physical Activity: Avoid strenuous exercise 24 hours before testing as it can temporarily modify lipid and inflammatory marker levels
    • Stress Reduction: Minimize emotional stress before testing as stress hormones may transiently elevate inflammatory markers and lipid levels
    • Timing of Testing: Morning testing (6-8 AM) is preferred after overnight fasting for optimal standardization and accuracy
    • Recent Illness Considerations: If patient has had acute infection, illness, or acute coronary event within 3 months, hs-CRP may be artificially elevated; ideally test 3 months after acute illness for baseline inflammation assessment
    • Menstrual Cycle: Women may test at any point in menstrual cycle; hormonal fluctuations minimally affect most lipid panel components except slight triglyceride variations
    • Hormone Therapy: Note if patient is on hormone replacement therapy or oral contraceptives as these may elevate triglycerides; consistent timing of testing recommended for monitoring purposes
    • Specimen Collection: Venous blood collection in serum separator tube (SST) or EDTA tube depending on laboratory preference; proper sample handling and timely processing essential for accurate results

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