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Biomedical subjects

A Jounela

Publications and source records attributed to A Jounela.

At least 19 recordsLinked to original sources
PubMed1999

Plasma vasoactive peptides after acute myocardial infarction in relation to left ventricular dysfunction.

We measured plasma concentrations of vasoactive peptides in 32 patients with acute myocardial infarction and evaluated their value as markers of left ventricular dysfunction. Plasma levels of atrial natriuretic peptide (ANP), the N-terminal fragment of proANP (NT-proANP), B-type natriuretic peptide (BNP) and endothelin-1 were measured serially by radioimmunoassays. The infarct size was estimated from the creatine kinase MB release curve. Coronary angiography and left ventricular cineangiography were performed in all patients during hospitalization and 6 months later in 15 patients. Myocardial infarction caused an increase in vasoactive peptides, the highest values for ANP (36.5+/-6.79 pmol/l), NT-proANP (1130+/-170 pmol/l) and endothelin-1 (9.72+/-0.68 pmol/l) being found on admission and those for BNP (56.0+/-7.13 pmol/l) on Day 2. Plasma levels of natriuretic peptides were dependent on infarct size, its location and degree of myocardial dysfunction and that of BNP also on infarct artery patency. Plasma endothelin-1 level was higher in patients with TIMI 3 than TIMI 0-2 flow. Plasma vasoactive peptides remained elevated during the 6-month follow-up period and they were dependent on the degree of myocardial dysfunction. BNP measured on any day of hospitalization showed the best correlation with ejection fraction measured during the acute phase of infarction or at 6 months. The results show that BNP is the best indicator of left ventricular dysfunction after myocardial infarction and its reliability is not dependent on the time point of measurement.

Analysis of Variance↗
PubMed1997

Collagen scar formation after acute myocardial infarction: relationships to infarct size, left ventricular function, and coronary artery patency.

BACKGROUND: Left ventricular function after acute myocardial infarction (AMI) is determined by the expansion of the infarct zone and remodeling of the noninfarcted myocardium. An occluded infarct-related artery (IRA) is an independent risk factor for remodeling. METHODS AND RESULTS: Changes in myocardial collagen metabolism were evaluated in 36 patients with suspected AMI. The plasma creatine kinase MB fraction and myoglobin release curves were analyzed for assessment of early reperfusion and infarct size. Collagen scar formation was evaluated by measurement of serum concentrations of the aminoterminal propeptide of type III procollagen (PIIINP), the aminoterminal propeptide of type I procollagen (intact PINP), and the carboxyterminal propeptide of type I procollagen (PICP). Plasma renin activity and urine excretion of cortisol and aldosterone were also measured. Coronary angiography and left ventricular cineangiography were performed during early hospitalization. The serum concentration of PIIINP increased from 3.50+/-0.20 to a maximum of 5.08+/-0.36 microg/L (n=32) in the patients with AMI, whereas the concentrations of intact PINP and PICP tended to decrease. The area under the curve (AUC) of PIIINP during the first 10 postinfarction days was larger in patients with severe heart failure or ejection fractions < or = 40% than in those with no heart failure or with an ejection fraction > 40% (P<.05 and P<.01, respectively), and it was also larger in the patients with TIMI grade 0 to 2 flows than in those with TIMI 3 flows (P<.05), despite similar enzymatically determined infarct sizes. No significant correlations between PIIINP and neurohumoral parameters were observed. The AUC of PIIINP and the change in PIIINP during the first 4 days were significantly correlated with indices of cardiac function. CONCLUSIONS: Collagen scar formation after AMI can be quantified by measurement of serum PIIINP concentrations. Scar formation is more prominent in large infarctions causing left ventricular dysfunction and in patients with occluded IRAs.

Adult↗
PubMed1996

Changes in interstitial collagen metabolism during acute myocardial infarction treated with streptokinase or tissue plasminogen activator.

Collagen plays a specific role in the maintenance of vascular integrity and in the thrombosis and scar formation processes. Therefore we found it interesting to study the changes in interstitial collagen metabolism during acute myocardial infarction treated with thrombolytic agents. Changes in collagen synthesis were evaluated by obtaining assays of the serum concentrations of the carboxyterminal propeptide of type I procollagen. Except fibrin plasmin is capable of degrading extracellular matrix components including collagen, and this capability was evaluated by monitoring the serum concentrations of the aminoterminal propeptide of type III procollagen. Twenty-four patients with suspected acute myocardial infarction and indications for thrombolytic therapy were randomized to receive either streptokinase (n = 11) or tissue plasminogen activator (n = 13). The patient groups were identical in their clinical characteristics. Serum levels of the aminoterminal propeptide of type III collagen increased rapidly on infusion of the thrombolytic agents, with the maximal mean increases of 44% and 16% in the streptokinase and TPA-treated groups, respectively. Levels of the carboxyterminal propeptide of type I collagen did not change during the thrombolytic therapy. A transient decrease occurred in the type I propeptide concentration at postinfarction day 2, and this decrease was followed by a secondary increase at days 4 to 6 in both patient groups studied. We conclude that thrombolytic agents stimulate the breakdown of interstitial collagen and that the collagen-degrading activity of TPA is lower than that of streptokinase. This factor may contribute to the relatively higher rethrombosis rate seen after TPA, because exposed collagen in the affected vascular wall stimulates thrombosis formation. On the other hand, increased collagen degradation followed by inhibition of collagen synthesis in the infarcted myocardium might increase the risk for cardiac rupture, especially after streptokinase treatment.

Antithrombins↗
PubMed1994

Effects of early administration of enalapril on radionuclide left ventricular ejection fraction and plasma N-terminal atrial natriuretic peptide after acute myocardial infarction.

The effects of enalapril therapy on radionuclide ejection fraction and plasma N-terminal atrial natriuretic peptide were investigated in a randomized, double-blind, placebo-controlled study of 52 patients with acute myocardial infarction. The medication was begun intravenously within 24 hours of the onset of symptoms. At discharge and the end point of 6 months, the radiographic size of the heart was significantly smaller in patients receiving (n = 28) than in those not receiving (n = 24) enalapril therapy (p < 0.03 vs < 0.01). However, left ventricular ejection fraction decreased simultaneously from 50 +/- 10% to 47 +/- 11% in patients treated with enalapril, whereas it increased from 48 +/- 13% to 50 +/- 14% in control patients (p < 0.05 for the difference of the changes). The decrease in ejection fraction was most marked in the infarct-related region of the left ventricle (p < 0.01). During the in-hospital period, plasma N-terminal atrial natriuretic peptide was decreased in patients treated with enalapril, whereas it was increased in those treated with placebo with complicated acute myocardial infarction (p < 0.05). During the following 6 months, the differences remained insignificant. Early administration of enalapril significantly attenuated heart enlargement after myocardial infarction and probably improved hemodynamics during the acute phase of complicated infarction. The decrease in ejection fraction during recovery indicates an impairment of systolic function. The decrease in infarct-related regional ejection fraction suggests that the impairment may be due to poor healing of the infarction scar.

Aged↗
PubMed1994

Plasma N-terminal atrial natriuretic peptide in acute myocardial infarction.

Plasma atrial natriuretic peptide (ANP) and the N-terminal (NT) fragment of the 126-amino acid prohormone of ANP (proANP; NT-proANP) were correlated with clinical findings in 41 patients with acute myocardial infarction and in 19 patients with angina pectoris. On admission to the hospital, the 39 patients with nonfatal infarction who subsequently had overt heart failure (n = 8) had plasma NT-proANP (2374 +/- 1038 pmol/L) and ANP (54 +/- 43 pmol/L) concentrations that were higher (p < 0.01) than those in the patients who remained without or who presented with minor signs of failure. In contrast to the relatively stable NT-proANP levels, ANP decreased markedly during the first 24 hours in the patients who had any signs of failure. Hence the plasma levels of NT-proANP and ANP did not go hand in hand in acute myocardial infarction, and NT-proANP appeared to be a better marker of cardiac dysfunction than ANP.

Aged↗
PubMed1992

A comparative study of nicardipine and pindolol as second-line treatments in essential hypertension.

A controlled, randomized, single-blind, parallel-group study compared the effects of nicardipine hydrochloride/hydrochlorothiazide (HCTZ) with those of pindolol/HCTZ in treatment of essential hypertension. The study included 43 patients aged 30-64 years with supine diastolic blood pressures between 95 and 125 mmHg at baseline. Patients initially received 50 mg/day HCTZ for 6 weeks and those patients whose diastolic blood pressure remained at or above 90 mmHg at week 6 (n = 29) completed a 6-week comparative phase in which they were given, in addition, either 30 mg nicardipine hydrochloride or 5 mg pindolol three times daily. Nicardipine was more effective than pindolol as a second-line treatment in controlling blood pressure but, because patients who were treated with nicardipine/HCTZ had higher baseline blood pressures, significance was lost when results were adjusted for the baseline blood pressure values. Treatment was described as 'very good' by 71.4% of patients in the nicardipine/HCTZ group and by 53.9% of those in the pindolol/HCTZ group; thus, both second-line antihypertensives were well accepted. Although 45% of patients in of each treatment group reported treatment-related adverse events, none experienced postural hypotension and no adverse event was unexpected.

Adult↗
PubMed1991

Thrombolytic therapy with streptokinase stimulates collagen breakdown.

BACKGROUND: Plasmin is capable of degrading extracellular matrix components such as collagen in vitro. To evaluate the significance of this for in vivo conditions, we set out to study the effect of streptokinase, which acts by converting plasminogen to plasmin, on the serum concentrations of the amino-terminal propeptide of type III procollagen (PIIINP) and the carboxy-terminal propeptide of type I procollagen (PICP). METHODS AND RESULTS: Twenty-three patients with suspected acute myocardial infarction were included in the study; 17 of them received thrombolytic therapy, and six were treated conservatively. PIIINP and PICP were assayed with radioimmunoassays. Kinetics of creatine kinase-MB release were determined to differentiate reperfusers from nonreperfusers. Composite curves of creatine kinase-MB release were constructed for different patient subgroups. During streptokinase infusion the serum concentrations of PIIINP increased rapidly, with a maximum mean increase of 50% (from 2.2 +/- 0.2 to 3.3 +/- 0.3 micrograms/l) in 45 minutes. A similar increase was also observed in two patients who received thrombolytic therapy but did not subsequently develop any myocardial infarction determined on the basis of enzyme release. The relative increase in PIIINP during streptokinase treatment was higher in those acute myocardial infarction patients with probable reperfusion than those with nonprobable reperfusion. Corresponding changes in PIIINP were not seen in the control group. Two days later there was a second increase in serum PIIINP for both patient groups. This change coincided with a similar increase in PICP. CONCLUSIONS: We conclude that streptokinase, probably by activation of plasminogen to plasmin, stimulates the breakdown of type III collagen during thrombolytic therapy. This phenomenon may decrease the risk of rethrombosis of the affected artery if the exposed collagen is responsible for thrombosis formation, but it could also be involved in the development of hemorrhagic complications during thrombolytic therapy. The second increase in PIIINP levels probably indicates type III collagen synthesis of the infarcted area. This investigation represents a pilot study, and more studies on the effects of various thrombolytic agents on interstitial collagen metabolism are obviously needed.

Collagen↗