Myocardial infarct size and mortality in patients with non-insulin-dependent diabetes mellitus

Abstract. Objectives. To study the infarct size and mortality in patients with non-insulin-dependent diabetes mellitus (NIDDM) and in non-diabetic subjects with their first acute myocardial infarction. Design. Seven year follow-up study of large representative cohorts of patients with non-insulin-dependent diabetes mellitus and non-diabetic subjects (study 1) and the FINMONICA acute myocardial infarction register study in 1988-89 (study 2). Setting. Populations of the districts of the Kuopio University Hospital and Turku University Central Hospital (study 1). Populations of Kuopio and North Karelia provinces and Turku/Loimaa area (study 2). Subjects. Study 1: 1059 patients with non-insulin dependent diabetes mellitus and 1373 non-diabetic subjects aged 45–64 years at baseline; during the follow-up 166 patients with non-insulin-dependent diabetes mellitus (91 men and 75 women) and 30 non-diabetic subjects (25 men and five women) were hospitalized for their first acute myocardial infarction. Study 2: 1622 patients aged 25–64 years hospitalized for their first acute myocardial infarction; 144 patients (90 men and 54 women) had non-insulin-dependent diabetes mellitus and 1153 (890 men and 263 women) were non-diabetic. Main outcome measures. The infarct size was assessed on the basis of maximum levels of serum cardiac enzymes (studies 1 and 2) and QRS-score (study 1). Results. No differences were found in maximum levels of serum cardiac enzymes between diabetic and non-diabetic patients. Similarly QRS-score gave no suggestion of a difference in infarct size between diabetic and non-diabetic patients. In both studies mortality before hospital admission was similar in diabetic and non-diabetic patients, but mortality within 28 days from hospital admission was twice as high in diabetic patients as in non-diabetic patients. Cardiac failure was the main cause of death significantly more often in diabetic patients than in non-diabetic patients (study 2). Conclusions. Poorer prognosis of acute myocardial infarction in diabetic patients appears not to be explained by a larger infarct size but probably by adverse effects of the diabetic state itself on myocardial function.     

Fatty acid composition of serum lipids in patients with a coronary bypass operation

The fatty acid composition of serum phospholipids and cholesteryl esters was analysed in 71 male patients with angiographically defined three-vessel coronary artery disease (CAD) selected for a coronary bypass operation. Their 71 control subjects were matched according to age, sex, smoking, relative weight, and absence of CAD. The concentrations of fatty acids, 14:0, 16:0 and 16:1 of the serum phospholipids, were significantly (P less than 0.01, P less than 0.05 and P less than 0.01, respectively) higher in CAD patients than in the controls. On the other hand, linoleic (18:2 omega 6), linolenic (18:3 omega 3) and arachidonic (20:4 omega 6) acids were at a significantly lower level in the patients when compared to the controls. The polyunsaturated/saturated fatty acids (P/S) ratio in serum phospholipids was significantly (P less than 0.01) lower in the patients than in the controls. In the cholesteryl ester fraction the results paralleled those of the phospholipids. Significant correlations were obtained between the polyunsaturated fatty acids and the high density lipoprotein cholesterol or apolipoprotein A-I in the control subjects but most of these correlations were absent in the patients. Our present results further support the importance of linoleic acid in the protection against atherosclerosis. However, no unequivocal evidence on the possible beneficial effect of long-chain omega 3-fatty acids in comparison with omega 6-acids was obtained.     

Molecular cloning, functional characterization of the porcine transient receptor potential V1 (pTRPV1) and pharmacological comparison with endogenous pTRPV1

In the present study, we cloned a porcine orthologue of transient receptor potential V1 (pTRPV1) and heterologously expressed it in human embryonic kidney (HEK) 293 cells to characterize its pharmacological properties. At the amino acid level, pTRPV1 was highly homologous (83-90%) to other orthologues of TRPV1. The expression of receptors was examined with current and [Ca2+]i responses to capsaicin using whole-cell patch-clamp and fura-2 ratio imaging techniques, respectively, and by immunostaining with an anti-TRPV1 antibody. The receptors were characterized by changes in [Ca2+]i in response to various vanilloid agonists, low pH and heat and by the effects of TRPV1 antagonists on them. The various TRPV1 agonists activated pTRPV1 in a dose-dependent manner in the order of potency of resiniferatoxin (RTX) > olvanil > capsaicin > phorbol 12-phenylacetate 13-acetate 20-homovanillate (PPAHV), phorbol 12,13-dinonanoate 20-homovanillate (PDNHV). Isovelleral and scutigeral had no effect. Endogenous vanilloids (anandamide > 15 (s)-HPETE > NADA), low pH and noxious heat (>42 degrees C) activated pTRPV1. Comparison of amino acid sequences with various mammalian TRPV1 homologues suggested some novel putative vanilloid recognition sites. TRPV1 antagonists, iodoRTX, ruthenium red and capsazepine suppressed capsaicin-induced responses. Similar to human TRPV1, but not rodent TRPV1, capsazepine was effective in blocking pH- and heat-induced responses. Similar pharmacological profiles were observed in cultured porcine dorsal root ganglion neurons. We discuss putative amino acid residues related to pharmacological differences among mammalian TRPV1 homologues.     

Coxsackie B Virus Antibodies in Myocardial Infarction

ABSTRACT. Evidence for the association between Coxsackie B virus infections and myocardial infarction was studied in a prospective follow-up examination. Using the micro neutralization test, 9 (15%) of 59 patients with acute myocardial infarction and 1 (2.6%) of 38 control patients showed a fourfold, or higher, antibody increase in paired serum samples against Coxsackie B1-5 viruses. This difference is significant (p≤0.05). None of the patients or controls revealed symptoms of a viral infection during the blood sampling. Virus isolation from throat and feces was negative in all patients and controls. This finding agrees with some previous studies suggesting that the Coxsackie B group may in some cases have a causal role in myocardial infarction, or may act as a triggering factor.     

OXIDATION OF GLUCOSE and D-B-OH-BUTYRATE BY THE EARLY HUMAN FETAL BRAIN

Abstract. Adam, P. A. J., Räihä, N., Rahiala, E.-L. and Kekomäki, M. (Departments of Pediatrics, Case Western Reserve University at Cleveland Metropolitan General Hospital, Cleveland, Ohio USA, and the University of Helsinki at the Children's Hospital, Helsinki, Finland). Oxidation of glucose and D-B-OH-butyrate by the early human fetal brain. Acta Paediatr Scand, 64:17, 1975.–The isolated brains of 12 previable human fetuses obtained at 12 to 21 weeks' gestation, were perfused through the interval carotid artery with glucose (3 mM) and/or DL-B-OH-butyrate (DL-BOHB), 4.5 mM, plus tracer quantities of either glucose-6-¹⁴C (G6¹⁴C) or β-OH-butyrate-3-¹⁴C (BOHB3¹⁴C). Oxidative metabolism was demonstrated by serial collection of gaseous ¹⁴CO₂ from the closed perfusion system, and from the recirculating medium. Glucose and BOHB were utilized at physiological rates as indicated (mean ±SEM): G6¹⁴C at 0.10±0.01 μmoles/min g brain (n=7) or 17.5±1.9 μmoles/ min kg fetus; and BOHB3¹⁴C at 0.16±0.05 μmoles/min g (n=5) or 27.3±7.4 μmoles/ min kg. Based on fetal weight, glucose metabolism by brain apparently accounted for about 1/3 of basal glucose utilization in the fetus. On a molar basis BOHB3¹⁴C was taken up at 1.47 times the rate of G6¹⁴C. Both BOHB3¹⁴C and G6 ¹⁴C were converted to ¹⁴C0₂. The rate of BOHB3¹⁴C conversion to ¹⁴CO₂ was equal to its rate of consumption, and exceeded the conversion of glucose to CO₂ because 45% of the G6¹⁴C was incorporated into lactate-¹⁴C. Accordingly, both substrates support oxidative metabolism by brain; and BOHB is a major potential alternate fuel which can replace glucose early in human development.     

Effect of Normal Human Serum on the Binding of Specific Antibodies and Platelet-unrelated Immune Complexes to Human Platelets

Radiolabelled staphylococcal protein A was used to quantitate the binding of IgG on stored human platelets from human sera containing specific antibodies reactive with platelets and rabbit serum containing immune complexes (IC). Normal human serum (NHS) inhibited the binding of IC onto platelets and to various extents also the binding of specific antibodies. The attachment of inhibitors to platelets seemed to be reversible. The considerable difference in the inhibitory capacities of IgG-deficient sera and monomeric IgG indicates that IgG is the major inhibitory component of NHS. The binding of IgG from NHS onto platelets evidently hampers the detection of weak platelet antibodies even with the most sensitive tests. Purified Clq, known to modify the reactions of IC with fresh platelets did not alter the binding of IC onto stored platelets. A monoclonal, antiglobulin-active rheumatoid factor of IgM class displayed only moderate inhibition. Therefore, the application of RF or Clq for the differentiation of the binding induced by IC or antibodies is not useful in this assay system. The heterogeneity of immunologic receptors of platelets provides an explanation of the inhibitory inefficiency of Clq.     

Impact of Occluded Culprit Arteries on Long‐Term Clinical Outcome in Patients with Non‐ST‐Elevation Myocardial Infarction: 48‐Month Follow‐Up Results in the COREA‐AMI Registry

Background

The prognostic impact of occluded culprit arteries in non‐ST‐elevation myocardial infarction (NSTEMI) patients beyond 12 months has not been investigated.

Objectives

The impact of occluded culprit arteries on a composite of cardiac death (CD), recurrent nonfatal MI (RMI), and target vessel revascularization (TVR) in patients who presented with NSTEMI was investigated during a 48‐month follow‐up using propensity‐score (PS) matching.

Methods

A total of 2,878 NSTEMI patients in the COREA‐AMI (COnvergent REgistry of cAtholic and chonnAm university for Acute MI) Registry were classified according to the angiographic flow of culprit arteries (occlusion [OC], n = 1,070; nonocclusion, n = 1,808). After PS matching, the incidence of the primary end‐point, a composite of CD, RMI, and TVR was compared.

Results

The median follow‐up duration was 47.3 months (IQR 32.7–66.2). In the PS‐matched population, the 48‐month cumulative rates of the primary end‐point (27.5% vs. 17.9%, P < 0.001) and each event were higher in the OC group (CD: 9.0% vs. 5.4%, RMI: 16.3% vs. 9.4%, TVR: 10.5% vs. 5.6%, respectively, P < 0.05). In multivariate Cox regression analysis, occluded culprit arteries showed the significant statistical impact on the primary end‐point (HR 1.689 [1.385–2.059], P < 0.001) and each event (CD: 1.736 [1.218–2.475], RMI: 1.918 [1.468–2.505], TVR: 2.042 [1.453–2.869], respectively, P < 0.05). Furthermore, in the 12‐month landmark analysis, occluded culprit arteries were still associated with higher risk of primary end‐point beyond 12 months (P < 0.001).

Conclusions

Occluded culprit arteries were independently associated with the higher risk of CD, RMI, and TVR in NSTEMI patients during the 48‐month follow‐up. (J Interven Cardiol 2014;27:12–20)