Giancarlo Marenzi

Centro Cardiologico Monzino, Milano, Lombardy, Italy

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Publications (115)592.97 Total impact

  • Ivana Marana, Giancarlo Marenzi, Amir Kazory
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    ABSTRACT: Despite major advances in pharmacological therapy and cardiac devices, heart failure patients continue to be frequently (re-)hospitalized with signs and symptoms of fluid overload. Diuretics improve the symptoms of fluid overload, but their effectiveness is reduced by a number of factors including excess salt intake, underlying chronic kidney disease, renal adaptation to their actions and neurohormonal activation. Ultrafiltration (UF) is a mechanical method of fluid removal with several potential advantages over diuretic-based conventional therapies: several recent studies have demonstrated favorable clinical response to UF therapy. Such studies have shown that removal of large amounts of isotonic fluid, in addition to relieving symptoms of congestion, can improve exercise capacity, reduce cardiac filling pressures, restore diuretic responsiveness, and portend a favorable effect on cardio-pulmonary, cardiorenal interactions, and neurohormonal hyperactivation. However, despite these proposed benefits, so far, no clinical study has yet been carried out to explore the impact of UF therapy on hard clinical endpoints such as long-term mortality. In this article, we review a number of mechanistic aspects of UF therapy, with particular emphasis on cardio-pulmonary and cardiorenal interactions, and revisit the results of more recent clinical trials in order to highlight the characteristics that can help identify patients who are more likely to benefit from this therapeutic modality.
    Nephrologie & therapeutique. 07/2014;
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    ABSTRACT: There are limited data comparing ultrafiltration with standard medical therapy as first-line treatment in patients with severe congestive heart failure (HF). We compared ultrafiltration vs. conventional therapy in patients hospitalized for HF and overt fluid overload. Patients with congestive HF were randomized to receive standard medical therapy (Control group) or ultrafiltration (Ultrafiltration group). The primary end point of the study was re-hospitalizations for congestive HF during a 1-year follow-up. Fifty-six patients were randomized to ultrafiltration (n=27) or standard therapy (n=29). Despite similar body weight reduction at hospital discharge in the two groups (7.5±4.5 and 7.9±5.0 kg, respectively; P=0.75), a lower incidence of re-hospitalizations for HF was observed in the ultrafiltration-treated patients during the following year (hazard ratio 0.14, 95% confidence interval 0.04-0.48; P=0.002). Ultrafiltration-induced benefit was associated with a more stable renal function, unchanged furosemide dose, and lower BNP levels. At one year, 7 (30%) deaths occurred in the ultrafiltration group, and 11 (44%) in the Control group (P=0.33). In HF patients with severe fluid overload, first-line treatment with ultrafiltration is associated with a prolonged clinical stabilization and a greater freedom from re-hospitalization for congestive HF.
    Journal of cardiac failure 11/2013; · 3.25 Impact Factor
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    ABSTRACT: To investigate whether admission B-type natriuretic peptide levels predict the development of acute kidney injury in acute coronary syndromes. Prospective study. Single-center study, 13-bed intensive cardiac care unit at a University Cardiological Center. Six-hundred thirty-nine acute coronary syndromes patients undergoing emergency and urgent percutaneous coronary intervention. None. We measured B-type natriuretic peptide at hospital admission in acute coronary syndromes patients (55% ST-elevation myocardial infarction and 45% non-ST-elevation myocardial infarction). Acute kidney injury was classified according to the Acute Kidney Injury Network criteria: stage 1 was defined as a serum creatinine increase greater than or equal to 0.3 mg/dL from baseline; stage 2 as a serum creatinine increase greater than two- to three-fold from baseline; stage 3 as a serum creatinine increase greater than three-fold from baseline, or greater than or equal to 4.0 mg/dL with an acute increase greater than 0.5 mg/dL, or need for renal replacement therapy. Acute kidney injury was developed in 85 patients (13%) and had a higher in-hospital mortality than patients without acute kidney injury (14% vs 1%; p < 0.001). B-type natriuretic peptide levels were higher in acute kidney injury patients than in those without acute kidney injury (264 [112-957] vs 98 [44-271] pg/mL; p < 0.001) and showed a significant gradient according to acute kidney injury severity (224 [96-660] pg/mL in stage 1 and 939 [124-1,650] pg/mL in stage 2-3 acute kidney injury; p < 0.001). The risk of developing acute kidney injury increased in parallel with B-type natriuretic peptide quartiles (5%, 9%, 15%, and 24%, respectively; p < 0.001). When B-type natriuretic peptide was evaluated, in terms of capacity to predict acute kidney injury, the area under the curve was 0.702 (95% CI, 0.642-0.762). In patients hospitalized with acute coronary syndromes, B-type natriuretic peptide levels measured at admission are associated with acute kidney injury as well as its severity.
    Critical care medicine 11/2013; · 6.37 Impact Factor
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    ABSTRACT: Rationale: Four monocentric studies reported that circadian rhythms can affect left ventricular infarct size after ST-segment-elevation acute myocardial infarction (STEMI). Objective: To further validate the circadian dependence of infarct size after STEMI in a multicentric and multiethnic population. Methods and Results: We analyzed a prospective cohort of subjects with first STEMI from the First Acute Myocardial Infarction study that enrolled 1099 patients (ischemic time <6 hours) in Italy, Scotland, and China. We confirmed a circadian variation of STEMI incidence with an increased morning incidence (from 6:00 am till noon). We investigated the presence of circadian dependence of infarct size plotting the peak creatine kinase against time onset of ischemia. In addition, we studied the patients from the 3 countries separately, including 624 Italians; all patients were treated with percutaneous coronary intervention. We adopted several levels of analysis with different inclusion criteria consistent with previous studies. In all the analyses, we did not find a clear-cut circadian dependence of infarct size after STEMI. Conclusions: Although the circadian dependence of infarct size supported by previous studies poses an intriguing hypothesis, we were unable to converge toward their conclusions in a multicentric and multiethnic setting. Parameters that vary as a function of latitude could potentially obscure the circadian variations observed in monocentric studies. We believe that, to assess whether circadian rhythms can affect the infarct size, future study design should not only include larger samples but also aim to untangle the molecular time-dynamic mechanisms underlying such a relation.
    Circulation Research 05/2013; 112(10):e110-4. · 11.86 Impact Factor
  • Giancarlo Marenzi, Nadia Aspromonte
    Journal of the American College of Cardiology 03/2013; · 14.09 Impact Factor
  • Marenzi G, Aspromonte N
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    ABSTRACT: letter
    Journal of the American College of Cardiology 01/2013; 13. · 14.09 Impact Factor
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    ABSTRACT: We examined circulating miRNA expression profiles in plasma of patients with coronary artery disease (CAD) vs. matched controls, with the aim of identifying novel discriminating biomarkers of Stable (SA) and Unstable (UA) angina. An exploratory analysis of plasmatic expression profile of 367 miRNAs was conducted in a group of SA and UA patients and control donors, using TaqMan microRNA Arrays. Screening confirmation and expression analysis were performed by qRT-PCR: all miRNAs found dysregulated were examined in the plasma of troponin-negative UA (n=19) and SA (n=34) patients and control subjects (n=20), matched for sex, age, and cardiovascular risk factors. In addition, the expression of 14 known CAD-associated miRNAs was also investigated. Out of 178 miRNAs consistently detected in plasma samples, 3 showed positive modulation by CAD when compared to controls: miR-337-5p, miR-433, and miR-485-3p. Further, miR-1, -122, -126, -133a, -133b, and miR-199a were positively modulated in both UA and SA patients, while miR-337-5p and miR-145 showed a positive modulation only in SA or UA patients, respectively. ROC curve analyses showed a good diagnostic potential (AUC ≥ 0.85) for miR-1, -126, and -483-5p in SA and for miR-1, -126, and -133a in UA patients vs. controls, respectively. No discriminating AUC values were observed comparing SA vs. UA patients. Hierarchical cluster analysis showed that the combination of miR-1, -133a, and -126 in UA and of miR-1, -126, and -485-3p in SA correctly classified patients vs. controls with an efficiency ≥ 87%. No combination of miRNAs was able to reliably discriminate patients with UA from patients with SA. This work showed that specific plasmatic miRNA signatures have the potential to accurately discriminate patients with angiographically documented CAD from matched controls. We failed to identify a plasmatic miRNA expression pattern capable to differentiate SA from UA patients.
    PLoS ONE 01/2013; 8(11):e80345. · 3.53 Impact Factor
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    ABSTRACT: Acute kidney injury (AKI) occurs frequently in patients with acute coronary syndromes (ACS) and is associated with adverse short- and long-term outcomes. To date, however, no standardized definition of AKI has been used for patients with ACS. As a result, information on its true incidence and the clinical and prognostic relevance according to the severity of renal function deterioration are still lacking. We retrospectively studied 3,210 patients with ACS. AKI was identified on the basis of the changes in serum creatinine during hospitalization according to the AKI Network criteria. Overall, 409 patients (13%) developed AKI: 262 (64%) had stage 1, 25 (6%) stage 2, and 122 (30%) stage 3 AKI. In-hospital mortality was greater in patients with AKI than in those without AKI (21% vs 1%; p <0.001). The adjusted risk of death increased with increasing AKI severity. Compared to no AKI, the adjusted odds ratio for death was 3.5 (95% confidence interval 1.79 to 6.83) with stage 1 AKI and 31.2 (95% confidence interval 16.96 to 57.45) with stage 2 to 3 AKI. A significant parallel increase in major adverse cardiac events was also observed comparing patients without AKI and those with stage 2 to 3 AKI. In conclusion, in patients with ACS, AKI is a frequent complication, and the graded increase of its severity, as assessed using the AKI Network classification, is associated with a progressive increased risk of in-hospital morbidity and mortality.
    The American journal of cardiology 12/2012; · 3.58 Impact Factor
  • Giancarlo Marenzi, Angelo Cabiati, Emilio Assanelli
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    ABSTRACT: Chronic kidney disease (CKD) is associated with a high burden of coronary artery disease. In patients with acute coronary syndromes (ACS), CKD is highly prevalent and associated with poor short- and long-term outcomes. Management of patients with CKD presenting with ACS is more complex than in the general population because of the lack of well-designed randomized trials assessing therapeutic strategies in such patients. The almost uniform exclusion of patients with CKD from randomized studies evaluating new targeted therapies for ACS, coupled with concerns about further deterioration of renal function and therapy-related toxic effects, may explain the less frequent use of proven medical therapies in this subgroup of high-risk patients. However, these patients potentially have much to gain from conventional revascularization strategies used in the general population. The objective of this review is to summarize the current evidence regarding the epidemiology and the clinical and prognostic relevance of CKD in ACS patients, in particular with respect to unresolved issues and uncertainties regarding recommended medical therapies and coronary revascularization strategies.
    World journal of nephrology. 10/2012; 1(5):134-145.
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    ABSTRACT: Radiological procedures utilizing intravascular iodinated contrast media are being widely applied for both diagnostic and therapeutic purposes and represent one of the main causes of contrast-induced nephropathy (CIN) and hospital-acquired renal failure. Although the risk of CIN is low (0.6-2.3 %) in the general population, it may be very high (up to 50 %) in selected subsets, especially in patients with major risk factors such as advanced chronic kidney disease and diabetes mellitus, and in those undergoing emergency percutaneous coronary interventions (PCI). Due to the lack of any effective treatment, prevention of this iatrogenic disease, which is associated with significant in-hospital and long-term morbidity and mortality and increased costs, is the key strategy. However, prevention of CIN continues to elude clinicians and is a main concern during PCI, as patients undergoing these procedures often have multiple comorbidities. The purpose of this study is to examine the pathophysiology, risk factors and clinical course of CIN, as well as the most recent studies dealing with its prevention and potential therapeutic interventions, especially during PCI.
    Internal and Emergency Medicine 10/2012; 7 Suppl 3:181-3. · 2.35 Impact Factor
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    ABSTRACT: Local renal ischemia is regarded as an important factor in the development of contrast-induced nephropathy (CIN). Mannose-binding lectin (MBL) is involved in the tissue damage during experimental ischemia/reperfusion injury of the kidneys. The aim of the present study was to investigate the association of MBL deficiency with radiocontrast-induced renal dysfunction in a large prospective cohort. 246 patients with advanced non-dialysis-dependent renal dysfunction who underwent radiographic contrast procedures were included in the study. Baseline serum MBL levels were analyzed according to the occurrence of a creatinine-based (increase of ≥0.5 mg/dL or ≥25% within 48 hours) or cystatin C-based (increase of ≥10% within 24 hours) CIN. The incidence of creatinine-based and cystatin C-based CIN was 6.5% and 24%, respectively. MBL levels were not associated with the occurrence of creatinine-based CIN. However, patients that experienced a cystatin C increase of ≥10% showed significantly higher MBL levels than patients with a rise of <10% (median 2885 (IQR 1193-4471) vs. 1997 (IQR 439-3504)ng/mL, p = 0.01). In logistic regression analysis MBL deficiency (MBL levels≤500 ng/ml) was identified as an inverse predictor of a cystatin C increase ≥10% (OR 0.34, 95% CI 0.15-0.8, p = 0.01). MBL deficiency was associated with a reduced radiocontrast-induced renal dysfunction as reflected by the course of cystatin C. Our findings support a possible role of MBL in the pathogenesis of CIN.
    BMC Nephrology 09/2012; 13:99. · 1.64 Impact Factor
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    ABSTRACT: Rationale: At the onset of ST-elevation acute myocardial infarction (STEMI), patients can present with very elevated circulating interleukin IL6(+)levels or very low IL6(-)levels. Objective: We compared these two groups of patients to understand whether it is possible to define specific STEMI phenotypes associated with outcome based on the cytokine response. Methods and Results: We compared 109 patients with STEMI in the top IL6 level (median 15.6 pg/ml; IL6(+)STEMI) with 96 in the bottom IL6 level (median 1.7 pg/ml; IL6(-)STEMI) and 103 matched controls extracted from the multi-ethnic First Acute Myocardial Infarction Study. We found minimal clinical differences between the IL6(+)STEMI and IL6(-)STEMI. We assessed the inflammatory profiles of the two STEMI groups and the controls by measuring 18 cytokines in blood samples. We exploited clustering analysis algorithms to infer the functional modules of interacting cytokines. IL6(+)STEMI patients were characterized by the activation of two modules of interacting signals comprising (a)IL10, IL8, MIP1α and C-reactive protein and (b)MCP1, MIP1β and MIG. IL10 was increased both in IL6(+)STEMI and IL6(-)STEMI patients compared with controls. IL6(+)IL10(+)STEMI patients had an increased risk of systolic dysfunction at discharge and of death at six months in comparison with IL6(-)IL10(+)STEMI patients. We combined IL10 and MIG (derived from the two identified cytokine modules) with IL6 in a formula yielding a risk-index that outperformed any single cytokine in prediction of systolic dysfunction and death. Conclusions: We have identified a characteristic circulating inflammatory cytokine pattern in STEMI patients that is not related to the extent of the myocardial damage. The simultaneous elevation of IL6 and IL10 levels distinguishes STEMI patients with worse clinical outcomes from other STEMI patients. These observations could have potential implications for risk-oriented patient stratification and for immune-modulating therapies.
    Circulation Research 08/2012; · 11.86 Impact Factor
  • Monica De Metrio, Valentina Milazzo, Giancarlo Marenzi
    Clinical Research in Cardiology 04/2012; 101(9):771-2. · 3.67 Impact Factor
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    JACC. Cardiovascular Interventions 04/2012; 5(4):455-6. · 1.07 Impact Factor
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    ABSTRACT: The evaluation of patients admitted at the emergency department (ED) for chest pain is challenging and involves many different clinical specialists including emergency physicians, laboratory professionals and cardiologists. The preferable approach to deal with this issue is to develop joint protocols that will assist the clinical decision-making to quickly and accurately rule-out patients with non life-threatening conditions that can be considered for early and safe discharge or further outpatient follow-up, rule-in patients with acute coronary syndrome and raise the degree of alert of the emergency physicians on non-cardiac life-threatening emergencies. The introduction of novel biomarkers alongside the well-established troponins might support this process and also provide prognostic information about acute short-term or chronic long-term risk and severity. Among the various biomarkers, copeptin measurement holds appealing perspectives. The utility of combining troponin with copeptin might be cost-effective due to the high negative predictive value of the latter biomarker in the rule-out of an acute coronary syndrome. Moreover, in the presence of a remarkably increased concentration (e.g., more than 10 times the upper limit of the reference range), to reveal the presence of acute life-threatening conditions that may not necessarily be identified with the use of troponin alone. The aim of this article is to review current evidence about the clinical significance of copeptin testing in the ED as well as its appropriate placing within diagnostic protocols.
    Clinical Chemistry and Laboratory Medicine 02/2012; 50(2):243-53. · 3.01 Impact Factor
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    ABSTRACT: The most effective regimen for the prevention of contrast-induced nephropathy (CIN) remains uncertain. Our purpose was to compare two regimens of sodium bicarbonate with 24 h sodium chloride 0.9% infusion in the prevention of CIN. We performed a prospective, randomized trial between March 2005 and December 2009, including 258 consecutive patients with renal insufficiency undergoing intravascular contrast procedures. Patients were randomized to receive intravenous volume supplementation with either (A) sodium chloride 0.9% 1 mL/kg/h for at least 12h prior and after the procedure or (B) sodium bicarbonate (166 mEq/L) 3 mL/kg for 1 h before and 1 mL/kg/h for 6 h after the procedure or (C) sodium bicarbonate (166 mEq/L) 3 mL/kg over 20 min before the procedure plus sodium bicarbonate orally (500 mg per 10 kg). The primary endpoint was the change in estimated glomerular filtration rate (eGFR) within 48 h after contrast. Secondary endpoints included the development of CIN. The maximum change in eGFR was significantly greater in Group B compared with Group A {mean difference -3.9 [95% confidence interval (CI), -6.8 to -1] mL/min/1.73 m2, P = 0.009} and similar between groups C and B [mean difference 1.3 (95% CI, -1.7-4.3) mL/min/1.73 m(2), P = 0.39]. The incidence of CIN was significantly lower in Group A (1%) vs. Group B (9%, P = 0.02) and similar between Groups B and C (10%, P = 0.9). Volume supplementation with 24 h sodium chloride 0.9% is superior to sodium bicarbonate for the prevention of CIN. A short-term regimen with sodium bicarbonate is non-inferior to a 7 h regimen. ClinicalTrials.gov Identifier: NCT00130598.
    European Heart Journal 01/2012; 33(16):2071-9. · 14.10 Impact Factor
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    ABSTRACT: Neutrophils are involved in thrombus formation. We investigated whether specific features of neutrophil activation characterize patients with acute coronary syndromes (ACS) compared to stable angina and to systemic inflammatory diseases. The myeloperoxidase (MPO) content of circulating neutrophils was determined by flow cytometry in 330 subjects: 69 consecutive patients with acute coronary syndromes (ACS), 69 with chronic stable angina (CSA), 50 with inflammation due to either non-infectious (acute bone fracture), infectious (sepsis) or autoimmune diseases (small and large vessel systemic vasculitis, rheumatoid arthritis). Four patients have also been studied before and after sterile acute injury of the myocardium (septal alcoholization). One hundred thirty-eight healthy donors were studied in parallel. Neutrophils with normal MPO content were 96% in controls, >92% in patients undergoing septal alcoholization, 91% in CSA patients, but only 35 and 30% in unstable angina and AMI (STEMI and NSTEMI) patients, compared to 80%, 75% and 2% of patients with giant cell arteritis, acute bone fracture and severe sepsis. In addition, in 32/33 STEMI and 9/21 NSTEMI patients respectively, 20% and 12% of neutrophils had complete MPO depletion during the first 4 hours after the onset of symptoms, a feature not observed in any other group of patients. MPO depletion was associated with platelet activation, indicated by P-selectin expression, activation and transactivation of leukocyte β2-integrins and formation of platelet neutrophil and -monocyte aggregates. The injection of activated platelets in mice produced transient, P-selectin dependent, complete MPO depletion in about 50% of neutrophils. ACS are characterized by intense neutrophil activation, like other systemic inflammatory syndromes. In the very early phase of acute myocardial infarction only a subpopulation of neutrophils is massively activated, possibly via platelet-P selectin interactions. This paroxysmal activation could contribute to occlusive thrombosis.
    PLoS ONE 01/2012; 7(6):e39484. · 3.53 Impact Factor
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    ABSTRACT: This study investigated the effect of furosemide-forced diuresis and intravenous saline infusion matched with urine output, using a novel dedicated device designed for contrast-induced nephropathy (CIN) prevention. CIN is a frequent cause of acute kidney injury associated with increased morbidity and mortality. A total of 170 consecutive patients with chronic kidney disease (CKD) undergoing coronary procedures were randomized to either furosemide with matched hydration (FMH group, n = 87) or to standard intravenous isotonic saline hydration (control group; n = 83). The FMH group received an initial 250-ml intravenous bolus of normal saline over 30 min followed by an intravenous bolus (0.5 mg/kg) of furosemide. Hydration infusion rate was automatically adjusted to precisely replace the patient's urine output. When a urine output rate >300 ml/h was obtained, patients underwent the coronary procedure. Matched fluid replacement was maintained during the procedure and for 4 h post-treatment. The definition of CIN was a ≥25% or ≥0.5 mg/dl rise in serum creatinine over baseline. In the FMH group, no device- or therapy-related complications were observed. Four (4.6%) patients in the FMH group developed CIN versus 15 (18%) controls (p = 0.005). A lower incidence of cumulative in-hospital clinical complications was also observed in FMH-treated patients than in controls (8% vs. 18%; p = 0.052). In patients with CKD undergoing coronary procedures, furosemide-induced high urine output with matched hydration significantly reduces the risk of CIN and may be associated with improved in-hospital outcome. (Induced Diuresis With Matched Hydration Compared to Standard Hydration for Contrast Induced Nephropathy Prevention [MYTHOS]; NCT00702728).
    JACC. Cardiovascular Interventions 01/2012; 5(1):90-7. · 1.07 Impact Factor
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    ABSTRACT: Mechanisms linking chronic kidney disease (CKD) and adverse outcomes in acute coronary syndromes (ACS) are not fully understood. Among potential key players, reduced nitric oxide (NO) synthesis due to its endogenous inhibitors, asymmetric (ADMA) and symmetric (SDMA) dimethylarginine could be involved. We measured plasma concentration of arginine, ADMA and SDMA and investigated their relationship with CKD and long-term outcome in non-ST-elevation myocardial infarction (NSTEMI). We prospectively measured arginine, ADMA, and SDMA at hospital admission in 104 NSTEMI patients. CKD was defined as an estimated glomerular filtration rate (eGFR) <60 ml/min/1.73 m(2). We considered a primary end point of combined cardiac death and re-infarction at a median follow-up of 21 months. In CKD (n = 33) and no-CKD (n = 71) patients, arginine and ADMA were similar, whereas SDMA was significantly higher in CKD patients (0.65±0.23 vs. 0.42±0.12 µmol/L; P<0.0001). Twenty-four (23%) patients had an adverse cardiac event during follow-up: 12 (36%) were CKD and 12 (17%) no-CKD patients (P = 0.02). When study population was stratified according to arginine, ADMA and SDMA median values, only SDMA (median 0.46 µmol/L) was associated with the primary end-point (P = 0.0016). In models adjusted for age, hemoglobin and left ventricular ejection fraction, the hazard ratio (HR) for CKD and SDMA were high (HR 2.93, interquartile range [IQR] 1.15-7.53; P = 0.02 and HR 6.80, IQR 2.09-22.2; P = 0.001, respectively) but, after mutual adjustment, only SDMA remained significantly associated with the primary end point (HR 5.73, IQR 1.55-21.2; P = 0.009). In NSTEMI patients, elevated SDMA plasma levels are associated with CKD and worse long-term prognosis.
    PLoS ONE 01/2012; 7(11):e48499. · 3.53 Impact Factor
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    ABSTRACT: This study sought to assess the prevalence of normal levels of high sensitivity C-reactive protein (hsCRP) at the very onset of ST-segment elevation myocardial infarction (STEMI). Levels of hsCRP ≥2 mg/l identify individuals who benefit from lipid lowering and possibly anti-inflammatory agents, but how many patients develop infarction in spite of hsCRP levels <2 mg/l and thus would be ineligible for these treatments? We studied 887 patients with unequivocally documented STEMI as the first manifestation of coronary disease and 887 matched control subjects from urban areas of Italy, Scotland, and China. Blood samples were obtained before reperfusion strategies <6 h from symptoms onset in order to limit acute event-related increases. hsCRP values were similar in samples obtained <2 h, 2 to 4 h, and 4 to 6 h from symptoms onset in all ethnic groups, consistent with the delayed hsCRP elevation after myocardial necrosis and thus indicative of pre-infarction levels. Median hsCRP values were significantly higher in patients than in control subjects: 2.49 (interquartile range [IQR]: 1.18 to 5.55) mg/l versus 1.32 (IQR: 0.58 to 3.10) mg/l (p < 0.0001), which is consistent with previous findings. However, 41% of patients had hsCRP levels <2 mg/l and conversely, 37% of control subjects had values ≥2 mg/l. The measurement of hsCRP, with a 2 mg/l cutoff, would not have predicted 41% of unequivocally documented STEMIs in 3 ethnic groups without evidence of previous coronary disease, thus indicating both its limitations as an individual prognostic marker and as an indicator of a generalized inflammatory pathogenetic component of STEMI. New specific prognostic and therapeutic approaches should be found for such a large fraction of patients at risk.
    Journal of the American College of Cardiology 12/2011; 58(25):2654-61. · 14.09 Impact Factor

Publication Stats

2k Citations
592.97 Total Impact Points

Institutions

  • 2000–2014
    • Centro Cardiologico Monzino
      Milano, Lombardy, Italy
  • 2011–2012
    • Università Vita-Salute San Raffaele
      Milano, Lombardy, Italy
  • 2009
    • Medical College of Wisconsin
      Milwaukee, Wisconsin, United States
  • 1988–2009
    • University of Milan
      • Institute of Human Physiology II
      Milano, Lombardy, Italy
  • 2008
    • Lund University
      • Department of Radiology
      Lund, Skane, Sweden
  • 2006
    • Ospedale di San Raffaele Istituto di Ricovero e Cura a Carattere Scientifico
      Milano, Lombardy, Italy
  • 1997–2000
    • National Research Council
      Roma, Latium, Italy
  • 1998
    • IRCCS Multimedica
      Milano, Lombardy, Italy
  • 1994–1998
    • Università degli Studi del Sannio
      Benevento, Campania, Italy