Modifications of protein Z and interleukin-6 during the acute phase of coronary artery disease.
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Acute Disease↗
Biomedical subjects
Rosanna Abbate
Publications and source records attributed to Rosanna Abbate.
Role of glycoprotein Ia gene polymorphisms in determining platelet function in myocardial infarction patients undergoing percutaneous coronary intervention on dual antiplatelet treatment.
Response variability to antiplatelet treatment has been described and the widespread use of acetylsalicylic acid (ASA) and clopidogrel requires clarification of the residual platelet reactivity (RPR). Various glycoprotein Ia (GpIa) polymorphisms have been investigated, but their influence on platelet reactivity in myocardial infarction (MI) patients undergoing percutaneous coronary intervention (PCI) on dual antiplatelet treatment is not still elucidated. Aim of this study was to evaluate the effect of C807T, G873A and T837C polymorphisms of GpIa on modulating platelet function in MI patients on dual antiplatelet treatment undergoing PCI. We measured platelet function by both a point-of-care assay (PFA100) and platelet-rich-plasma aggregation in 289 MI patients undergoing PCI and receiving dual antiplatelet treatment. Our data show that C807T/G873A polymorphisms, but not T837C, are associated with higher platelet reactivity. Carriers of the 807T/873A allele had significantly higher platelet aggregation values after arachidonic acid (AA) and collagen stimuli and, even if they did not reach the statistical significance, after 2 and 10 microM ADP stimuli; 807T/873A allele carriers had also significantly shorter closure times on PFA100/epinephrine membranes. At the multiple analyses, C807T/G873A polymorphisms resulted an independent risk factor for RPR defined by both AA induced platelet aggregation (OR=3.0, 95%CI 1.17-7.89, p=0.022) or by PFA100/epinephrine (OR=4.1, 95%CI 1.53-10.89, p=0.005). In conclusion, this study shows the 807T/873A allele of the GpIa gene is an independent risk factor for the RPR on dual antiplatelet treatment, and extends, in a larger acute coronary syndrome population, the observation that the 807T/873A allele is associated with higher platelet reactivity.
Adult↗
Coffee consumption and risk of coronary heart disease: a meta-analysis.
BACKGROUND AND AIMS: During the past three decades the relationship between habitual coffee drinking and coronary heart disease (CHD) has been assessed in numerous studies, with conflicting results. The aim of this study was to systematically examine the data published on the association between habitual coffee consumption and risk of CHD. METHODS AND RESULTS: Thirteen case-control and 10 cohort studies were included. Case-control studies incorporated 9487 cases of CHD and 27,747 controls, and cohort studies included a total of 403,631 participants that were followed for between 3 and 44 years. The summary of odds ratios (OR) for the case-control studies showed statistically significant associations between coffee consumption and CHD for the highest intake group (>4 cups/day), OR 1.83 (95% CI 1.49-2.24; P<0.0001), and for the second highest category (3-4 cups/day), OR 1.33 (95% CI 1.04-1.71; P<0.0001), while no significant association emerged for low daily coffee intake (< or =2 cups/day), OR 1.03 (95% CI 0.87-1.21; P=0.45). The analysis of long-term follow-up cohort studies did not show any association between the consumption of coffee and CHD, with a relative risk (RR) of 1.16 (95% CI 0.95-1.41; P=0.14) for the highest category, and 1.05 (95% CI 0.90-1.22; P=0.57) and 1.04 (95% CI 0.90-1.19; P=0.60) for the second and third highest categories, respectively. These results did not differ substantially when controlling for region of origin, fatal and non-fatal events, year of publication, and number of years of follow-up. CONCLUSIONS: Despite a significant association between high consumption of coffee and CHD reported among case-control studies, no significant association between daily coffee consumption and CHD emerged from long-term follow-up prospective cohort studies.
Adult↗
Lone and secondary nonvalvular atrial fibrillation: role of a genetic susceptibility.
BACKGROUND: An involvement of the renin angiotensin system in atrial fibrillation (AF) has been hypothesized, and ACE DD genotype has been suggested to influence the predisposition to AF. The aim of this study was to investigate the role of the ACE I/D polymorphism in relation to the different clinical forms of AF, lone and secondary nonvalvular atrial fibrillation (NVAF). METHODS: 510 consecutive patients with documented NVAF (106 patients had lone, and 404 secondary NVAF), and 520 controls with a negative history of cardiovascular disease have been studied. RESULTS: A significant difference in allele frequency between lone and secondary NVAF (p=0.002) has been found. The ACE D allele was associated with the predisposition to lone NVAF under a dominant, recessive and additive model, both at univariate and multivariate analysis, after adjustment for age and gender (multivariate analysis: dominant OR=2.87, p=0.02; recessive OR=2.01, p=0.003; additive OR=4.47, p<0.0001). ACE D allele was significantly associated with secondary NVAF at both univariate and multivariate analysis under a recessive and additive, but not dominant, model (multivariate analysis: recessive OR=1.89, p=0.001; additive OR=2.50, p<0.0001). CONCLUSIONS: This study highlights the role of ACE gene in predisposing to both lone and secondary NVAF, further contributing to penetrate the genetic mechanisms responsible for this complex disease. The clinical relevance of our results may be related to the possible characterization of subjects predisposed to NVAF in the absence of traditional risk factors, and to the use of ACE-inhibitors therapy able to improve the arrhythmogenic substrate.
Aged↗
Genetic susceptibility to atrial fibrillation (AF) in patients with congestive heart failure.
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Alleles↗
Usefulness of aspirin resistance after percutaneous coronary intervention for acute myocardial infarction in predicting one-year major adverse coronary events.
Recently, great interest has focused on the phenomenon of aspirin resistance, which may be defined as clinical or laboratory resistance. Monitoring the antiplatelet effect appears to be relevant in the presence of clinical implications, but no data are available on the possible clinical implications of the failure of aspirin to inhibit tests of platelet function in the setting of acute coronary syndromes. This study evaluated the role of aspirin resistance in the occurrence of 1-year major adverse coronary events (MACEs) in patients with acute myocardial infarction (AMI) who have undergone percutaneous coronary intervention (PCI). We prospectively evaluated 146 patients (115 men and 31 women; median age 65 years, range 30 to 84) with AMI who underwent primary PCI. Exclusion criteria were the use of glycoprotein IIb/IIIa inhibitors, hematocrit <or=30%, and a platelet count <100,000/mm3. Platelet function analyzer-100 closure times by collagen-epinephrine were used for measuring platelet function in venous blood samples obtained 12 to 15 hours after revascularization. Patients were considered aspirin resistant in the presence of a collagen-epinephrine closure time of <203 seconds. After 1-year follow-up, MACEs were recorded in 44 of 146 patients (30.1%). A significantly higher percentage of patients with MACEs had aspirin resistance (39.1% vs 23.2%, p <0.05). A Kaplan-Meier survival curve showed that the overall risk of MACEs was significantly higher among patients with aspirin resistance (p = 0.02). A Cox regression analysis that adjusted for age, gender, traditional cardiovascular risk factors, systolic left ventricular function, number of stenosed coronary arteries, and previous AMI, PCI, or coronary artery bypass graft showed aspirin resistance to be a significant and independent risk factor for the future MACEs (hazard ratio 2.9, 95% confidence interval 1.1 to 9.2, p <0.05). In conclusion, our data demonstrate that aspirin resistance after PCI is a significant and independent predictor of MACEs in patients with AMI undergoing primary PCI.
Adult↗
A model of anti-angiogenesis: differential transcriptosome profiling of microvascular endothelial cells from diffuse systemic sclerosis patients.
The objective of this work was to identify genes involved in impaired angiogenesis by comparing the transcriptosomes of microvascular endothelial cells from normal subjects and patients affected by systemic sclerosis (SSc), as a unique human model disease characterized by insufficient angiogenesis. Total RNAs, prepared from skin endothelial cells of clinically healthy subjects and SSc patients affected by the diffuse form of the disease, were pooled, labeled with fluorochromes, and hybridized to 14,000 70 mer oligonucleotide microarrays. Genes were analyzed based on gene expression levels and categorized into different functional groups based on the description of the Gene Ontology (GO) consortium to identify statistically significant terms. Quantitative PCR was used to validate the array results. After data processing and application of the filtering criteria, the analyzable features numbered 6,724. About 3% of analyzable transcripts (199) were differentially expressed, 141 more abundantly and 58 less abundantly in SSc endothelial cells. Surprisingly, SSc endothelial cells over-express pro-angiogenic transcripts, but also show up-regulation of genes exerting a powerful negative control, and down-regulation of genes critical to cell migration and extracellular matrix-cytoskeleton coupling, all alterations that provide an impediment to correct angiogenesis. We also identified transcripts controlling haemostasis, inflammation, stimulus transduction, transcription, protein synthesis, and genome organization. An up-regulation of transcripts related to protein degradation and ubiquitination was observed in SSc endothelial cells. We have validated data on the main anti-angiogenesis-related genes by RT-PCR, western blotting, in vitro angiogenesis and immunohistochemistry. These observations indicate that microvascular endothelial cells of patients with SSc show abnormalities in a variety of genes that are able to account for defective angiogenesis.
Biopsy↗
Analysis of minK and eNOS genes as candidate loci for predisposition to non-valvular atrial fibrillation.
AIM: Mink protein, a beta-subunit of I(ks) potassium channels modulate cardiac cellular electrophysiology, and experimental data demonstrated that NO is involved in cardiac vagal activity and in the inhibition of sympathetic activity. We evaluated the role of eNOS -786T>C, 894G>T, 4a/4b and of minK S38G polymorphisms as predisposing factors to non-valvular atrial fibrillation (NVAF). METHODS AND RESULTS: We studied 331 consecutive patients with documented NVAF and in 441 control subjects, comparable for age and gender. A significant difference in allele frequencies between patients and controls for minK S38G and eNOS -786T>C, but not for eNOS 894G>T and 4a/4b polymorphisms, was observed. The minK 38G allele was significantly associated with susceptibility to NVAF at both univariate and multivariable analysis, according to dominant and recessive genetic model (multivariable analysis, dominant: OR=1.73, P=0.004 and recessive: OR=1.59, P=0.006). The eNOS -786C allele weakly influenced NVAF at univariate analysis, according to the dominant model (OR=1.50, P=0.01). The contemporary presence of minK 38G and eNOS -786C alleles increased the predisposition to NVAF, after adjustment with cardiovascular risk factors (OR minK 38G*eNOS -786C=2.11, P<0.0001; OR=2.58, P=0.003; OR=3.08, P=0.002, according to dominant, recessive, and additive model, respectively). CONCLUSION: Our findings suggest a role for minK and eNOS genes as predisposing factors to NVAF.
Aged↗
Predictors of vitamin B6 and folate concentrations in older persons: the InCHIANTI study.
BACKGROUND: Low dietary intake and low serum concentrations of vitamin B6 and/or folate are associated with increased risk of vascular events, possibly because of their association with inflammation, which plays a crucial role in the pathogenesis of cardiovascular diseases. METHODS: Using data from 1320 participants in the population-based InCHIANTI study (586 men and 734 women; median age, 69 years; range, 21-102 years) for whom complete data on folate, vitamin B6, inflammatory markers, 5,10-methylenetetrahydrofolate reductase (MTHFR) C677T sequence variant, and important covariates were available, we evaluated the association of inflammatory markers with circulating concentrations of vitamin B6 and folate, independently of dietary vitamin intake, circulating vitamin concentrations, and MTHFR C677T sequence variant. RESULTS: According to multiple linear regression analysis, C-reactive protein and interleukin-6 receptor were strongly and negatively associated with circulating vitamin B6 but not with folate concentrations, independent of age, sex, serum creatinine, serum albumin, total energy intake, smoking history, dietary nutrient intake, and circulating homocysteine and vitamin concentrations. Serum folate concentrations were related to MTHFR 677 TT genotype in persons with folate intake in the lowest tertile (< 221.2 microg/day). Vitamin C and retinol intakes were strongly and positively associated with serum folate concentrations independent of age, sex, serum creatinine, serum albumin, total energy intake, smoking history, homocysteine plasma concentrations, dietary nutrient intakes, serum vitamin B6 and vitamin B12 concentrations, and MTHFR C677T sequence variant. CONCLUSIONS: Low serum vitamin B6, but not serum folate, concentrations are independent correlates of the proinflammatory state, and both are influenced by antioxidant reserves.
Adult↗
Hyperviscosity as a possible risk factor for cerebral ischemic complications in atrial fibrillation patients.
Recent studies have suggested that hyperviscosity is frequent in patients with atrial fibrillation (AF). The aims of this study were to evaluate if hemorheologic alterations play a role in the occurrence of cerebral ischemic events in patients with AF and to explore a possible association between inflammation and hyperviscosity in these patients. Sixty-two patients with AF with a history of >or=1 cerebral ischemic event and 94 patients with AF without cerebral ischemic events were studied. A control population included 130 age- and gender-matched healthy volunteers. Hemorheologic variables (whole-blood viscosity, plasma viscosity, the erythrocyte deformability index, and hematocrit), fibrinogen, and high-sensitivity C-reactive protein levels were assayed. An alteration in whole blood viscosity at 94.5 seconds(-1) and the erythrocyte deformability index were found more frequently in patients with previous ischemic events on univariate and multivariate analyses (odds ratio 3.19, p=0.023 and odds ratio 4.26, p=0.002, respectively) adjusted for age, gender, hypertension, diabetes, history of coronary artery disease, left ventricular dysfunction, smoking habit, dyslipidemia, hematocrit, fibrinogen, high-sensitivity C-reactive protein, and hemorheologic parameters. These results should stimulate prospective studies on the role of hemorheologic alterations in the occurrence of cerebral ischemic complications in patients with AF.
Aged↗
Hyperhomocysteinemia and hypercoagulability in primary biliary cirrhosis.
AIM: To assess the hypercoagulability in PBC and its relationship with homocysteine (HCY) and various components of the haemostatic system. METHODS: We investigated 51 PBC patients (43F/8M; mean age: 63+/-13.9 yr) and 102 healthy subjects (86 women/16 men; 63+/-13 yr), and evaluated the haemostatic process in whole blood by the Sonoclot analysis and the platelet function by PFA-100 device. We then measured HCY (fasting and after methionine loading), tissue factor (TF), thrombin-antithrombin complexes (TAT), D-dimer (D-D), thrombomodulin (TM), folic acid, vitamin B6 and B12 plasma levels. C677T 5,10-methylenetetrahydrofolate reductase (MTHFR) polymorphism was analyzed. RESULTS: Sonoclot RATE values of patients were significantly (P<0.001) higher than those of controls. Sonoclot time to peak values and PFA-100 closure times were comparable in patients and controls. TAT, TF and HCY levels, both in the fasting and post-methionine loading, were significantly (P<0.001) higher in patients than in controls. Vitamin deficiencies were detected in 45/51 patients (88.2%). The prevalence of the homozygous TT677 MTHFR genotype was significantly higher in patients (31.4%) than in controls (17.5%) (P<0.05). Sonoclot RATE values correlated significantly with HCY levels and TF. CONCLUSION: In PBC, hyper-HCY is related to hypovitaminosis and genetic predisposing factors. Increased TF and HCY levels and signs of endothelial activation are associated with hypercoagulability and may have an important role in blood clotting activation.
Adult↗
Exaggerated local hand sympathetic but not renin-angiotensin system activation in patients with primary Raynaud's phenomenon.
In Raynaud's disease (RD), an overactivity of sympathetic nervous system (SNS) was hypothesized but only indirect proofs were obtained. Complex interactions between the renin-angiotensin system (RAS) and SNS were reported without clear demonstrations of a RAS involvement. Recently, the use of ACE inhibitors and AT1 receptor antagonists in RD patients showed mixed results. The study of total and regional kinetics of tritiated noradrenaline (NA) and the measurements of local Angiotensin (Ang) I and II arterial-venous gradient were performed in 10 RD patients and 10 controls both in rest conditions and following a cold pressor test (CPT). Hand blood flow (HBF) was measured by strain-gauge plethysmography. Baseline HBF was slightly lower in patients than in controls, but during CPT, it significantly decreased only in RD patients (P < 0.01). Total (3H)-NA clearance and spillover were similar in the two groups throughout the study. On the contrary, baseline hand NA spillover was higher in RD patients than in controls and the difference further increased during CPT. Hand NA spillover was linearly related to HBF (P < 0.001). Arterial-venous Ang I and Ang II gradients were positive without difference between controls and patients throughout the study. In conclusion in RD patients, a pathological waste of NA from sympathetic nervous endings of the hand region, exaggerated by sympathetic stimulation, occurs but an enhanced local Ang II formation was not demonstrable.
Case-Control Studies↗
Low adherence of a clinically healthy Italian population to nutritional recommendations for primary prevention of chronic diseases.
BACKGROUND AND AIM: Several data demonstrated that dietary habits significantly affect the health state of the population. During recent years all the major scientific associations have provided nutritional recommendations for primary prevention of chronic diseases but few data are available about prevalence of adherence to these recommendations in an otherwise healthy population. The aims of this study were to evaluate dietary habits, and to assess the adherence of the general population to the recommendations for correct nutritional behaviour. METHODS AND RESULTS: Dietary habits, anthropometric and biochemical parameters were evaluated in a population of 932 (367 M; 565 F) clinically healthy subjects living in Florence, enrolled in an epidemiologic study conducted between 2002 and 2004. By comparing the dietary pattern with the nutritional guidelines, the study population reported a hyperproteic and hyperlipidic nutritional pattern, with a considerably low contribution from polyunsaturated fats (PUFA). A low fibre intake is shown in both genders. In addition, food consumption pattern showed an increased consumption of some foods such as meat, both fresh and processed, and a low intake of some "healthy" foods like fruit and vegetables. CONCLUSIONS: We found several nutritional flaws in the dietary habits of a clinically healthy Italian population. In particular, we reported a high intake of animal protein and total fats with a very low contribution from PUFA.
Adult↗
Hemorheologic profile in systemic sclerosis: role of NOS3 -786T > C and 894G >T polymorphisms in modulating both the hemorheologic parameters and the susceptibility to the disease.
OBJECTIVE: Microvascular disorders are relevant in systemic sclerosis (SSc). Hyperviscosity, due to alterations of blood cells and plasma components, may play a role in the pathogenesis of microcirculatory disorders. An impaired availability of nitric oxide, related to polymorphisms in NOS3, the gene for endothelial cell nitric oxide synthase, might influence erythrocyte deformability. We undertook this study to investigate the hemorheologic profile in SSc and the role of NOS3 polymorphisms in modulating the hemorheologic status of SSc patients. METHODS: We studied 113 consecutive SSc patients (75 with limited cutaneous SSc [lcSSc] and 38 with diffuse cutaneous SSc [dcSSc]) and 113 healthy controls. The hemorheologic profile was obtained by assessing whole blood viscosity (WBV; at shear rates of 0.512 and 94.5 seconds(-1)), plasma viscosity (PLV; at a shear rate of 94.5 seconds(-1)), and erythrocyte deformability index (DI). We determined NOS3 polymorphisms by molecular analysis. RESULTS: A marked alteration of hemorheologic parameters was found both in patients with lcSSc and in those with dcSSc compared with controls (P < 0.0001). In multivariate analysis, rheologic variables were significantly associated with the disease (for WBV at a shear rate of 94.5 seconds(-1), odds ratio [OR] 5.4, 95% confidence interval [95% CI] 1.4-19.9, P = 0.01; for PLV, OR 2.8, 95% CI 1.2-6.5, P = 0.01; for DI, OR 3.9, 95% CI 1.4-10.8, P = 0.007), and NOS3 -786C and 894T alleles significantly affected the DI (for -786C allele, OR 2.3, 95% CI 1.01-5.4, P = 0.04; for 894T allele, OR 2.2, 95% CI 1.01-4.8, P = 0.04). The simultaneous presence of the -786C and 894T alleles represented a susceptibility factor for SSc (OR 2.8, 95% CI 1.4-5.7, P = 0.004). CONCLUSION: Our findings document an altered rheologic profile in SSc and demonstrate a relationship between this alteration and NOS3 polymorphisms, thus shedding light on a potential novel mechanism influencing the microcirculation in this disease.
Aged↗
Endothelial nitric oxide synthase gene influences the risk of pre-eclampsia, the recurrence of negative pregnancy events, and the maternal-fetal flow.
OBJECTIVES: Pre-eclampsia is associated with vascular endothelial dysfunction, adverse pregnancy outcome and cardiovascular disease in later life. An inadequate nitric oxide availability related to polymorphisms in the endothelial nitric oxide synthase gene (eNOS) might predispose to the disease. METHODS: We investigated the role of eNOS T-786C, G894T and 4a4b polymorphisms in predisposing to both pre-eclampsia and the recurrence of negative pregnancy events, per se and in the presence of angiotensin-converting enzyme (ACE) DD genotype, and investigated their influence on maternal-fetal flow in 106 non-thrombophilic women with a history of pre-eclampsia, compared with 106 women with a history of normal pregnancy. RESULTS: No association between eNOS polymorphisms and predisposition to pre-eclampsia was found; nevertheless, the contemporary presence of eNOS 894TT and -786CC genotypes represented a susceptibility factor to the disease. In 48 out of 106 women, documented complications (pre-eclampsia and fetal growth restriction) were present in the current pregnancy. The eNOS 894TT genotype influenced the risk of recurrence of negative events (odds ratio = 5.45), particularly in contemporary women homozygous for both eNOS 894TT and ACE DD genotypes (odds ratio = 11.4). Throughout the pregnancy, a progressive alteration of maternal-fetal flow indices was found in women carrying the eNOS 894TT genotype, and this effect was strengthened in women with the contemporary presence of the ACE DD genotype. CONCLUSIONS: An original finding is the increased risk of pre-eclampsia and recurrence of pregnancy negative events, probably by modulating the maternal-fetal flow, in women homozygous for the eNOS 894T allele previously analyzed for the ACE I/D polymorphism.
Adult↗
Protein Z gene polymorphisms (intron F 79 G>A; -13 A>G) are not associated with acute coronary syndromes.
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Acute Disease↗
Angiotensin-converting enzyme in systemic sclerosis: from endothelial injury to a genetic polymorphism.
The main pathologic hallmark of systemic sclerosis (SSc) is endothelial derangement; the pathologic alterations of the vessel wall in SSc are strikingly similar to the modification detected in the atherosclerotic lesions, and it is now evident that SSc is also characterized by accelerated macrovascular disease. Peptides related to angiotensin II, the final product of the renin-angiotensin system (RAS), play a role as regulators of endothelial cell function. Angiotensin-converting enzyme (ACE), the key enzyme in the RAS, is the predominant pathway of angiotensin II formation in blood and tissues. In intron 16 of the gene encoding for ACE an insertion/deletion (I/D) polymorphism, consisting of the presence or absence of a 287-base pair Alu sequence, has been identified. This polymorphism has been related to ACE enzyme levels, and data from experimental studies reported a functional role for this polymorphism in modulating the angiotensin II levels. We previously documented a high ACE D allele frequency in SSc patients and its role in increasing the risk of SSc, thus suggesting that the I/D polymorphism might be a useful genetic marker to identify SSc patients at risk to develop a severe vascular disease, frequently leading to gangrene. Moreover, our preliminary data, besides supporting the role of ACE I/D polymorphism as a predisposing factor to SSc, demonstrated its involvement in accelerated macrovascular disease by increasing the intima media thickness. Therefore, in SSc, not only endothelial dysfunction, but also vascular damage, linked to ACE I/D polymorphism, may significantly contribute to accelerated macrovascular disease, as the ACE D allele, by regulating both the production of angiotensin II and the degradation of bradykinin, contributes to mechanisms involved in the induction and maintenance of vessel wall modification.
Angiotensin-Converting Enzyme Inhibitors↗
Protein Z levels and prognosis in patients with acute coronary syndromes.
BACKGROUND: Protein Z, a vitamin K-dependent glycoprotein, serves as a cofactor for the inhibition of activated coagulation factor X. During recent years, a role for low levels of protein Z in prothrombotic disorders such as ischemic stroke and acute coronary syndromes (ACS) has been reported. The aims of this study were to test changes in protein Z and their association with outcome at 1-year follow-up in 193 (150 male, 43 female) patients with ACS. RESULTS: Protein Z plasma levels were significantly lower (p<0.0001) after 1 year [1,600 (28-3,736) ng/mL] compared to the baseline [1,695 (294-4,068) ng/mL]. Regression analysis showed a significant association between baseline protein Z below the 5th percentile of our control group and subsequent adverse cardiac events at follow-up (odds ratio 3.3; 95% CI 1.04-10.7; p=0.04). Moreover, Cox regression analysis showed that low protein Z levels at admission were significant predictors of major adverse cardiac events (cardiac death, non-fatal recurrent myocardial infarction, and need for target lesion revascularization) after 1 year (hazard risk 2.5; 95% CI 1.02-6.5, p=0.04). CONCLUSIONS: Our results show that in patients with ACS: 1) protein Z decreases moving from the acute to the convalescent phase; and 2) low levels of baseline protein Z are significantly associated with adverse outcome at 1-year follow-up.
Acute Disease↗