Preventive Cardiology & Internal Medicine & Family Medicine & Rheumatology
hsCRP (high-sensitivity C-reactive protein)
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C-reactive protein (CRP) is an acute-phase protein synthesized by the liver in response to IL-6, the main hepatic cytokine inducing the inflammatory response. In its standard version, CRP is used to detect acute inflammatory or infectious conditions (values >10 mg/L). High-sensitivity CRP (hsCRP) is the same analyte measured by an immunometric technique with very high analytical sensitivity, capable of detecting concentrations as low as 0.1-0.3 mg/L - i.e. 10 to 100 times below the detection threshold of standard CRP. This precision makes it possible to measure chronic low-grade inflammation, a sub-clinical state associated with atherosclerosis progression, atherosclerotic plaque instability and cardiovascular events. Since the pioneering work of Paul Ridker in the late 1990s, hsCRP has been recognized as one of the best-validated cardiovascular inflammatory biomarkers: it independently predicts the risk of myocardial infarction, stroke, sudden death and peripheral arterial disease in the general population, even in people with normal or low LDL cholesterol. The JUPITER trial (2008) demonstrated that, in patients with hsCRP ≥2 mg/L and LDL <3.4 mmol/L, treatment with rosuvastatin reduced major cardiovascular events by 44 % - legitimizing hsCRP as a decision-making tool for initiating statin therapy in a specific subgroup. Nevertheless, hsCRP remains a marker, not a direct therapeutic target, and its routine clinical use is subject to debate - its measurement being recommended in specific contexts of intermediate cardiovascular risk stratification, not as a routine screening test.
Biology, sources, and determinants of hsCRP
- Structure, synthesis, and physiological role of CRP: molecular structure: CRP = 118 kDa pentameric (annular) protein → 5 identical non-glycosylated subunits → synthesized exclusively by hepatocytes → CRP gene located on chromosome 1q23.2 → native pentameric structure (pCRP) → can dissociate into monomers (mCRP) during local inflammatory states - notably in atherosclerotic plaque → mCRP = more pro-inflammatory form than pCRP → Black 2004 - Arteriosclerosis, Thrombosis, and Vascular Biology: mCRP activates complement + stimulates release of MCP-1 (monocyte chemoattractant protein) → recruitment of monocytes to plaque; regulation of hepatic synthesis: main stimulus: IL-6 (interleukin-6) → produced by adipocytes + macrophages + endothelial cells + smooth muscle cells → activation of JAK/STAT3 + NF-κB in hepatocytes → CRP gene transcription → co-stimulators: IL-1β + TNF-α + leptin + angiotensin II → inhibitors: IL-10 + statins (partial inhibition of hepatic synthesis independently of LDL) + aspirin (weakly) + kinetics: half-life: 19 hours → onset of elevation: 4-6h after stimulus → peak at 24-72h → normalization: 3-7 days if stimulus resolved → in chronic low-grade inflammation: permanent, modest elevation (1-10 mg/L) → stable over weeks to months → good intra-individual reproducibility (intra-individual coefficient of variation: 30-40 % → justifies 2 measurements separated by 2 weeks in clinical practice); physiological roles of CRP: opsonization: CRP binds to phosphocholine in cellular debris + bacteria → complement activation (classical pathway via C1q) → phagocytosis facilitated → recognition and clearance of apoptotic and necrotic cells → in atherosclerosis: controversial role - activating CRP or simple marker? → Libby 2002 - New England Journal of Medicine: CRP → stimulates production of adhesion molecules (ICAM-1 + VCAM-1 + E-selectin) in endothelial cells → promotes monocyte adhesion → but : Mendelian randomization studies (Timpson 2005 - Arteriosclerosis, Thrombosis, and Vascular Biology + Zacho 2008 - NEJM) → genetic variants associated with chronic elevated CRP → no increase in cardiovascular risk → suggests that CRP is a biomarker of inflammation rather than a causal mediator of atherosclerosis
- Non-cardiovascular determinants of hsCRP — causes of elevation to know: not every elevation in hsCRP reflects increased cardiovascular risk - many non-cardiovascular causes elevate CRP and must be ruled out before interpreting hsCRP in a risk stratification context; acute and subacute infections: bacterial infections → very high CRP (often 50-200 mg/L) → well above cardiovascular stratification threshold → viral infections → moderate elevation → severe COVID-19: CRP often 50-150 mg/L → indicator of severity (Huang 2020 - Lancet) → abscess + sepsis → very high CRP; chronic systemic inflammatory diseases: rheumatoid arthritis (RA): chronically elevated hsCRP (2-50 mg/L) → doubling of cardiovascular risk independently (Peters 2004 - Arthritis and Rheumatism) + systemic lupus erythematosus + ankylosing spondylitis + IBD (Crohn's disease + ulcerative colitis) + psoriasis + vasculitis → in these pathologies: hsCRP reflects the inflammatory activity of the disease + increased cardiovascular risk → do not interpret hsCRP as a simple cardiovascular biomarker without context; obesity and metabolic syndrome: visceral adipose tissue produces large amounts of IL-6 → elevated hsCRP → obesity → hsCRP often 3-10 mg/L even without other cause → T2DM + insulin resistance → chronic inflammation → elevated hsCRP → Visser 1999 - Journal of the American Medical Association: obesity (BMI >30) → median hsCRP ×2-3 vs normal weight → hsCRP in this context is a marker of metabolic inflammation, not just cardiovascular; smoking: active smoking → increase in hsCRP by 1-3 mg/L (mechanism: activation of pulmonary macrophages + oxidative stress + activation of NF-κB) → Bazzano 2003 - American Journal of Epidemiology: smokers → hsCRP 1.5 × higher vs non-smokers → smoking cessation → progressive normalization in 3-6 months; non-alcoholic fatty liver disease (NAFLD/MASLD): liver inflammation → moderate CRP elevation → correlates with histological severity (steatosis → NASH → fibrosis) + alcoholism: CRP elevation even without cirrhosis; pregnancy: physiological increase in hsCRP especially in 3rd trimester + pre-eclampsia: very high hsCRP (marker of systemic endothelial dysfunction); hsCRP-lowering drugs: statins: 15-25 % reduction in hsCRP independent of LDL reduction → Ridker 2001 - Circulation: rosuvastatin, atorvastatin, pravastatin → median CRP reduction 25-37 % + fibrates (fenofibrate): moderate reduction + anti-TNF (infliximab + adalimumab): major reduction in RA and spondyloarthritis + tocilizumab (anti-IL-6R): almost complete normalization of hsCRP → methotrexate + hydroxychloroquine (RA) + aspirin (weakly) + GLP-1 agonists (semaglutide + liraglutide): 20-40 % reduction in hsCRP by reducing adipocyte inflammation (Ridker 2021 - New England Journal of Medicine: canakinumab and anti-inflammatory - CANTOS trial)
Reference values, risk stratification, and clinical use
| Domain / Application | Data, thresholds, and modalities | Key studies and recommendations |
|---|---|---|
| Reference Values and Cardiovascular Stratification Thresholds AHA/CDC — low risk — intermediate — high — reproducibility — pre-analytical |
AHA/CDC 2003 classification (Pearson 2003 - Circulation) for cardiovascular risk stratification by hsCRP: low risk: hsCRP 3.0 mg/L → value >10 mg/L: suggests an active infectious or inflammatory cause → to be repeated after resolution of confounding factor → upper limit of normal value in healthy asymptomatic general population: 0.5-1.0 mg/L depending on laboratory → median hsCRP in healthy North American adult population: 1.5-2.0 mg/L (Ridker 2003 - Circulation: WHS - Women's Health Study cohort) → reference percentiles in the general population: 50th percentile ≈ 1.5 mg/L + 75th percentile ≈ 3.0 mg/L + 90th percentile ≈ 7.0 mg/L; analytical methods - hsCRP vs standard CRP: standard CRP (turbidimetry or classical nephelometry): detection limit 5-10 mg/L → unusable for cardiovascular stratification → hsCRP (high-sensitivity immunonephelometry + high-sensitivity ELISA + high-sensitivity immunoturbidimetry): detection limit 0.1-0.3 mg/L → analytical co-efficient of variation: 10 mg/L → ideally 2 measurements 2 weeks apart → use the mean of the 2 values → sampling: serum or EDTA plasma → stable at room temperature 24h + 4°C 7 days + -20°C indefinitely → no significant circadian variation → no need to fast (hsCRP is not affected by meals, unlike LDL) → intra-individual variation (biological coefficient of variation): 30-40 % over 1 year → therefore: a single measurement is insufficient to definitively classify a patient → 2 measurements + clinical context recommended; factors that increase hsCRP and must be excluded before cardiovascular interpretation: recent infection (viral or bacterial) within 4-6 weeks → trauma + recent surgery → active chronic inflammatory disease → IBD or RA flare → active neoplasia → pregnancy → unbalanced diabetes + severe obesity (BMI >35) can raise hsCRP to levels (>3 mg/L) that mask or overestimate cardiovascular risk proper | Pearson 2003 - Circulation (AHA/CDC Scientific Statement): seminal document defining cardiovascular stratification thresholds for hsCRP + recommendations: hsCRP should be measured by standardized methods with high sensitivity + 2 measurements separated by 2 weeks if used for stratification + do not measure during acute illness + value >10 mg/L → repeat after resolution of acute condition + Ridker 2003 - Circulation (WHS - Women's Health Study): prospective cohort of 28,345 initially healthy women × 8 years → hsCRP independent predictor of cardiovascular risk superior to LDL-cholesterol → hsCRP + LDL → better stratification than each alone → first solid data in primary prevention in women + meta-analysis Danesh 2004 - NEJM (Emerging Risk Factors Collaboration): 22 prospective studies n=7,068 coronary cases → hsCRP increased by a factor of 3 → coronary risk OR 1.45 (CI 95 % 1.25-1.68) → association independent of traditional risk factors → but: modest added value to prediction by Framingham score alone (improved c-statistic of 0.76 → 0.77) → conclusion: hsCRP is a marker, not an isolated stratification tool |
| hsCRP and cardiovascular risk stratification — Reynolds score and JUPITER Reynolds Score — JUPITER — rosuvastatin — low LDL — hsCRP ≥ 2 mg/L — primary prevention |
Reynolds Risk Score - integration of hsCRP into stratification: developed by Paul Ridker + Nancy Cook (Ridker 2007 - JAMA for women + Ridker 2008 - Circulation for men) → improves prediction of 10-year cardiovascular risk compared with the Framingham score + Pooled Cohort Equations (PCE) → variables: age + sex + systolic blood pressure + LDL-cholesterol + HDL-cholesterol + hsCRP + smoking + family history of premature ischemic heart disease (father or mother <60 years) → contribution of hsCRP: 15-20 % reclassification of patients considered «intermediate risk» by Framingham score → some reclassified to higher risk → decision to treat → some to lower risk → avoid unnecessary treatment → Ridker 2007 - JAMA (WHS - Women's Health Study): n=24,558 women × 10 years → Reynolds Risk Score → net reclassification of 40-50 % intermediate-risk women by Framingham → significant improvement in discrimination (positive NRI) → Ridker 2008 - Circulation: Reynolds score validated in men (PHS II - Physicians Health Study) + c-statistic improvement of 0.756 → 0.774 → modest but statistically significant; JUPITER trial (Justification for the Use of Statins in Prevention: an Intervention Trial Evaluating Rosuvastatin) - founder trial: Ridker 2008 - NEJM: design: multicenter RCT × 26 countries + n=17,802 adults with no known cardiovascular disease + LDL <3.4 mmol/L (130 mg/dL) + hsCRP ≥2.0 mg/L → rosuvastatin 20 mg/d vs placebo → stopped prematurely after 1.9 years (median) because clear benefit → results: LDL reduction of 50 % + hsCRP reduction of 37 % → MACE reduction (MI + stroke + revascularization + cardiovascular death) of 44 % (HR 0.56 - IC 95 % 0.46-0.69) → fatal and non-fatal MI reduction: 54 % → stroke reduction: 48 % → VTE reduction: 43 % (additional anti-inflammatory effect of statins) → reduction in all-cause mortality: 20 % → NNT (number needed to treat) over 5 years: 25 patients to prevent 1 major event → NNT comparable to statins in secondary prevention → main conclusion: in patients with low LDL but chronic inflammation (hsCRP ≥2 mg/L), rosuvastatin is beneficial → legitimization of hsCRP as a therapeutic decision criterion; criticisms and limitations of JUPITER: premature termination of the trial → potential bias of benefit amplification → does the reduction in MACE reflect the anti-LDL effect or the anti-inflammatory effect? → impossible to dissociate (rosuvastatin simultaneously reduces LDL AND hsCRP) + Ridker himself: the beneficial effect is probably the sum of both effects → Everett 2013 - American Heart Journal: JUPITER post-hoc analysis → patients achieving LDL <1.8 mmol/L AND hsCRP <2 mg/L → reduction in MACE 65 % → dual LDL + hsCRP target → maximal benefit → failure to achieve hsCRP target despite rosuvastatin → lesser benefit → residual hsCRP on statin as marker of residual risk | Position of learned societies on the use of hsCRP in therapeutic decision-making: ACC/AHA 2019 Guidelines on Primary Prevention of Cardiovascular Disease (Arnett 2019 - Circulation): hsCRP can be used to refine the statin treatment decision in patients at intermediate cardiovascular risk (10-year risk of 7.5-20 % per PCE) whose decision is uncertain → hsCRP ≥2 mg/L in this setting → argument in favor of treatment → class IIa - level of evidence B → do not measure hsCRP in patients already at high risk (secondary or >20 % at 10 years) nor in patients at low risk (0 → cardiovascular risk RR 3.5-7.7 depending on value + CAC and hsCRP uncorrelated → measure different aspects of risk: CAC = anatomical atherosclerotic burden + hsCRP = chronic systemic inflammation → association CAC + hsCRP → optimal stratification → Ridker 2020 - Lancet: patients with CAC = 0 + high hsCRP → predominantly thrombotic risk + inflammation → no atherosclerosis → candidates for anti-inflammatory drugs + lifestyle modification rather than a statin |
| hsCRP and non-cardiovascular diseases — expanded clinical applications Rheumatoid arthritis — diabetes — cancer — heart failure — COPD — depression — CANTOS |
hsCRP as a transnosal biomarker of chronic inflammation: type 2 diabetes and metabolic syndrome: Pickup 1997 - BMJ: hsCRP predictive of type 2 diabetes in the IRAS cohort → Dehghan 2007 meta-analysis - Archives of Internal Medicine: elevated hsCRP → RR T2DM 1.63 (CI 95 % 1.49-1.78) → mechanism: chronic low-grade inflammation (adipokines + IL-6 + TNF-α) contributes to insulin resistance + beta-cell dysfunction → hsCRP is a marker of pre-diabetic state and insulin resistance → but: Mendelian randomization → genetically elevated CRP does not predict T2DM (Dehghan 2011 - Diabetologia) → CRP = marker of metabolic syndrome rather than causal factor; heart failure: Vasan 2006 - NEJM (Framingham): elevated hsCRP → increased risk of heart failure × 1.5-2 independently → hsCRP also predicts deterioration in systolic function → in established CI: hsCRP correlates with severity (NYHA) + predicts rehospitalization + mortality → Torre-Amione 1996 - Journal of the American College of Cardiology: elevated TNF-α + IL-6 in CHF → parallel hsCRP + CANTOS (Canakinumab Anti-Inflammatory Thrombosis Outcomes Study - Ridker 2017 - NEJM): groundbreaking trial → n=10,061 post-IDM patients with hsCRP ≥2 mg/L → canakinumab (anti-IL-1β monoclonal antibody - pure anti-inflammatory, no effect on LDL) vs placebo → reduction in hsCRP by 37 % → reduction in MACE by 15 % (HR 0.85 - CI 95 % 0.74-0.98) → major proof of concept: cardiovascular inflammation is an LDL-independent therapeutic target → notable side effect: increase in lethal infections (pneumonia + sepsis) → canakinumab has no cardiovascular indication (marginal risk/benefit) → but: major beneficial effect on lung cancer occurrence (67 % reduction in lung cancer mortality in subgroup) → Ridker 2016 - Lancet: result not expected - anti-inflammation = anti-tumor in this context; COPD: elevated hsCRP in 50 % of patients with stable COPD → predicts exacerbations + mortality → systemic inflammatory component of COPD → Sin 2003 - American Journal of Respiratory and Critical Care Medicine; rheumatoid arthritis (RA): hsCRP = marker of disease activity + additional cardiovascular risk factor in RA → Peters 2004 - Arthritis and Rheumatism: RA + elevated hsCRP → cardiovascular risk × 2 vs RA + normal hsCRP → RA treatment (methotrexate + anti-TNF + tocilizumab) → reduction in hsCRP → reduction in cardiovascular risk → Ridker 2021 - NEJM: colchicine (LoDoCo2 - Nidorf 2020 Lancet + COLCOT - Tardif 2019 NEJM): anti-inflammatory + hsCRP reduction of 10-20 % → MACE reduction of 23-31 % → cardiovascular anti-inflammatory alternative with favorable safety profile → colchicine 0.5 mg/d → multi-agency approval (FDA + Health Canada - NDA) for secondary cardiovascular prevention; depression and mental health: Howren 2009 meta-analysis - Psychosomatic Medicine: elevated hsCRP associated with depression (Cohen's d = 0.15) → chronic inflammation → neuroinflammation → depression? → or vice versa? → likely bidirectional model → no direct clinical application at present but active research avenue | Clinical implications of CANTOS and anti-inflammatory trials for practice: CANTOS 2017 - NEJM: evidence that cardiovascular inflammation (measured by hsCRP) is a causal therapeutic target (not just a marker) → validates Libby's inflammatory hypothesis of atherosclerosis → canakinumab not available in cardiovascular routine → but : COLCOT (Tardif 2019 - NEJM): colchicine 0.5 mg/d post-IDM → reduction MACE 23 % → LoDoCo2 (Nidorf 2020 - Lancet): colchicine 0.5 mg/d in chronic stable coronary artery disease → reduction MACE 31 % → colchicine is now approved by Health Canada (Lodoco - colchicine 0.5 mg) for secondary cardiovascular prevention → mechanism: inhibition of microtubule polymerization + inhibition of NLRP3 inflammasome complex + inhibition of IL-1β + IL-18 secretion → reduction of IL-6 → reduction of hsCRP → hsCRP can be used to identify patients likely to benefit from colchicine (high residual hsCRP on statin) → current clinical practice in Quebec: residual hsCRP >2 mg/L despite optimal statin + no active infection/inflammation → consider colchicine 0.5 mg/d + optimization of modifiable risk factors + eliminate secondary causes of elevated hsCRP |
| Prescription, interpretation, and clinical integration of hsCRP Indications — not routinely indicated — RAMQ — confounding causes — decision algorithm — LDL + hsCRP |
Validated indications for hsCRP assay in clinical practice: cardiovascular stratification in primary prevention in the intermediate-risk patient: calculated 10-year risk between 7.5 and 20 % (PCE) or 5-10 % (SCORE2 Europe) → decision to treat uncertain → hsCRP ≥2 mg/L → argument in favor of statin + patient with intermediate 10-year risk + family history of early coronary artery disease + hsCRP ≥2 mg/L → reinforcement of treatment decision + monitoring of efficacy of anti-inflammatory treatment (colchicine + statin) : hsCRP as secondary target → goal: hsCRP <2 mg/L under treatment → monitoring of systemic inflammatory disease activity (RA + IBD + APS) + patient with metabolic syndrome + T2DM at intermediate cardiovascular risk → hsCRP can reclassify risk; situations where hsCRP is not indicated or insufficient: patient already at high cardiovascular risk (history of MI + stroke + proven coronary artery disease + T2DM with target organ damage) → statin from the outset, no need for hsCRP → patient at low risk calculated at 10 years (<7,5 %) + asymptomatic → hsCRP result does not change management + fever + recent infection + active inflammatory disease → hsCRP not interpretable for cardiovascular risk + follow-up with standard CRP in acute infectious phase → use standard CRP (faster + less expensive + results in mg/L identical for high values) ; practical interpretation algorithm in Quebec : hsCRP 3.0 mg/L: high risk → but first check for non-cardiovascular causes (infection + inflammation + obesity + smoking) → if excluded : consider treatment (statin ± colchicine) + modify lifestyle factors + hsCRP >10 mg/L: acute cause to be identified before any cardiovascular interpretation → resume dosing after resolution; non-pharmacological strategies to reduce hsCRP: weight loss: 10 % reduction in body weight → 20-30 % reduction in hsCRP (Tchernof 2002 - Arteriosclerosis, Thrombosis, and Vascular Biology) + regular aerobic exercise (150 min/week): 15-25 % reduction in hsCRP (Kasapis 2005 - Journal of the American College of Cardiology) + Mediterranean diet: 20 % reduction in hsCRP - PREDIMED (Estruch 2013 - NEJM) + smoking cessation: reduction in hsCRP in 3-6 months + statins (rosuvastatin 20 mg): reduction of 37 % (JUPITER 2008) + colchicine 0.5 mg/d: reduction of 10-20 % + Ω-3 fatty acids (EPA + DHA >2 g/d): modest reduction in hsCRP - Mozaffarian 2011 - Circulation + fibrates: moderate reduction + tocilizumab + anti-TNF: major reduction in inflammatory diseases (not indicated only for cardiovascular hsCRP) | Reimbursement and availability in Quebec - RAMQ and practice: hsCRP (high-sensitivity C-reactive protein): assay available in all hospital and private laboratories in Quebec → result in mg/L → high-sensitivity immunonephelometric or immunoturbidimetric method → timeframe: same-day or D+1 result → RAMQ reimbursement: hsCRP reimbursed if medical prescription with documented indication → included in cardiovascular workup panels from certain laboratories (Dynacare + Biron + hospital laboratories) → cost without insurance: approx. 15-30 $ CAD → standard CRP and hsCRP are different assays → ensure that the laboratory measures hsCRP (high sensitivity) and not standard CRP if value <3 mg/L → explicitly request «hsCRP» or «high sensitivity CRP» on the prescription to avoid a standard CRP whose detection limit prevents cardiovascular stratification; integration with other cardiovascular biomarkers: LDL-cholesterol + hsCRP: combination recommended by ACC/AHA 2019 for stratification in the intermediate group → apolipoprotein B (apoB) + hsCRP: apoB measures atherogenic particle concentration + hsCRP measures inflammation → complementary → Lp(a) + hsCRP: high Lp(a) + high hsCRP → very high risk → argument for aggressive treatment → triglycerides + hsCRP: metabolic syndrome → both are often elevated together → CAC (coronary calcium) + hsCRP: optimal combination → CAC measures anatomical atherosclerosis + hsCRP measures inflammation → patients CAC = 0 + high hsCRP → mainly thrombotic + inflammatory risk → no subclinical atherosclerosis → colchicine + lifestyle → patients CAC high + normal hsCRP → advanced atherosclerosis without major inflammation → statin + aspirin depending on overall risk |
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A hsCRP >10 mg/L should suggest an acute infectious or inflammatory cause—not cardiovascular risk: hs-CRP can only be interpreted as a cardiovascular risk marker in the range of 1-10 mg/L, in the absence of any active infection or inflammatory disease. A value >10 mg/L suggests an infectious cause, a rheumatic flare-up, or a neoplasm, and should be re-checked after the acute episode has passed. Furthermore, hs-CRP is only useful in cardiovascular risk stratification for patients at intermediate risk where the decision to treat is uncertain—it is not a tool for routine screening.
Situations where a very high hs-CRP points towards an urgent cause to investigate
hsCRP >50-100 mg/L + fever + chills + altered general state → bacterial sepsis + severe infection (pneumonia + pyelonephritis + endocarditis + abscess) → medical emergencies → blood cultures + complete infectious workup → empirical antibiotics based on suspected source → hsCRP at these levels has no value for cardiovascular stratification.
High hsCRP >10 mg/L persistent on 2 spaced tests + weight loss + night sweats + enlarged lymph nodes + profound fatigue Neoplasm + lymphoma + disseminated tuberculosis → complete workup: CBC + LDH + thoraco-abdomino-pelvic CT scan + PET-CT if lymphoma is suspected → immediate medical consultation.
Elevated hsCRP + atypical chest pain + dyspnea + moderate fever in a young patient → acute pericarditis + myocarditis → ECG + troponin + echocardiography → urgent cardiology consultation → pericarditis → CRP often 30–100 mg/L → marker of pericardial inflammatory activity + guides duration of treatment (Imazio 2013 — NEJM: colchicine + aspirin in acute pericarditis → hsCRP normalization = criterion for recovery + 50% reduction in recurrences %).
Stable coronary patient on optimal statin therapy with persistent residual hsCRP >2 mg/L on 2 spaced measurements, after exclusion of infectious and inflammatory causes → Residual inflammatory cardiovascular risk → discussion of adding colchicine 0.5 mg/day (Lodoco — Health Canada approved) or intensifying lifestyle changes → cardiology or internal medicine consultation for treatment reevaluation.
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Les médecins de Clinique Omicron prescrivent et interprètent la hsCRP dans le cadre d'un bilan cardiovasculaire complet, intègrent ce marqueur avec le score de risque global, le LDL, l'apoB et les autres facteurs de risque pour guider les décisions thérapeutiques, et assurent le suivi des patients sous statines ou colchicine. Des consultations sont disponibles dans plusieurs points de service au Québec et en télémédecine. Pour prendre rendez-vous, choisissez votre service en ligne.
The content of this page is provided for informational purposes only and does not substitute professional medical advice. The interpretation of hsCRP should always be integrated into the patient's overall clinical context and does not, by itself, indicate a need for treatment.
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