Time course of serum collagen types I and III metabolism products after reperfused acute myocardial infarction in patients with and without systemic hypertension

Abstract

We examined 55 consecutive patients successfully treated with primary percutaneous coronary intervention (PCI) for a first acute myocardial infarction with left ventricular (LV) systolic dysfunction. In all patients we performed echocardiographic examination, dosage of plasma brain natriuretic peptide, serum carboxy-terminal propeptide and telopeptide of procollagen type I and amino-terminal propeptide of procollagen type III at days 1 and 3, and at 1 and 6 months after index infarction. The hypertensive patients (group 1; n ¼ 30) differed for higher baseline blood pressure (133±4 mm Hg vs 118±4 mm Hg; P ¼ 0.03), greater LV mass index (108 ± 5 vs 94 ± 4 g m À2 , P ¼ 0.03) and lower mitral E/A wave peak (0.8 ± 0.06 vs 1.1±0.12, P ¼ 0.02) with respect to non-hypertensive patients (group 2; n ¼ 25). From day 1 to month 6 carboxy-terminal propeptide of procollagen type I and amino-terminal propeptide of procollagen type III increased (Po0.005 and Po0.05, respectively) in both groups, whereas carboxy-terminal telopeptide of procollagen type I increased from day 1 to day 3 (Po0.01 in both groups, respectively) and then decreased from day 3 to month 6 (Po0.01 and Po0.05 in both groups, respectively). From day 1, brain natriuretic peptide decreased in both groups (Po0.005). There was no significant difference between the two groups in values of procollagens and natriuretic peptide. Finally, LV diastolic volume and function at 6 months were similar in the two groups. Thus, in patients with reperfused acute myocardial infarction and LV dysfunction, antecedent hypertension was not associated with a different pattern of serum procollagen release and ventricular remodelling at 6 months of follow-up.

The prognostic value of circulating markers of collagen turnover after acute myocardial infarction

“…Second, we collected blood samples at randomisation (median 3 [IQR2-5] days). As the release of CTO markers vary with time following AMI [10,24,30], a range of several days for the sampling times carries the potential risk that the assessed CTO markers fail to represent peak levels at the time of assessment. This may lead to an underestimation of the relationship between CTO markers and outcomes and therefore do not compromise our results.…”

“…These patients were assessed relatively late (mean 8.5 ± 2.8 days) following MI and all patients were on treatment with an angiotensin converting enzyme inhibitor (ACEi) or angiotensin II receptor blocker (ARB) at the time of initial assessment. Both the time-point of assessment following MI and the prescription of inhibitors of the renin-angiotensin-aldosterone-system (RAAS), have significant effects on levels of circulating collagens [10][11][12]. In clinical practice there is a need to evaluate patients early following MI, and many patients are not treated by RAAS inhibitors at the time of their first MI.…”

Effect of coronary revascularization on serum collagen biomarkers and left ventricular remodeling in patients with acute myocardial infarction

“…15 In patients with a first MI and LV dysfunction, the elevation of PICP and PIIINP may last for up to 6 months after a successful primary PCI. 16 During the early hours of MI, the increase in serum PIIINP is mainly caused by collagenolysis, whereas an enhanced synthesis of collagen seems to cause the elevation of PIIINP a few days after the MI. In the present study, the level of serum PIIINP on day 180 was higher than on day 7 in both groups of patients.…”

The novel diagnostic marker in low-LVEF heart failure patients

“…Also we didn't carry out serial measurements at the time of each hospitalization. Cerisano et al found that patients with acute myocardial infarction revealed persistant increment of PIP from day 1 to month 6, refl ecting the healing process of injured myocardium (15). Thus, new surge in the stationary level of increased PIP necessitates new cardiac events ending with fi brosis.…”