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Biomedical subjects

K Kanmatsuse

Publications and source records attributed to K Kanmatsuse.

At least 73 records · Page 4Linked to original sources
PubMed1999

Structure of the type B human natriuretic peptide receptor gene and association of a novel microsatellite polymorphism with essential hypertension.

The natriuretic peptide (NP) system may play a crucial role in development of essential hypertension (EH). C-type NP dilates arteries and lowers blood pressure and inhibits proliferation of vascular smooth muscle cells via the type B NP receptor (NPR-B). However, the association of the human NPR-B gene with EH has not been studied, because little is known about the genomic organization of this gene. We designed oligonucleotide primers based on the cDNA sequence of the human NPR-B gene, and long-range polymerase chain reaction (PCR) was performed. The amplified fragments were sequenced directly, and the exon/intron organization of the human NPR-B gene was determined. The gene, which spans approximately 16.5 kbp, is composed of 22 exons, and the intron-exon junctions follow the GT-AG rule. Seven hundred fifty base pairs of the 5'-flanking region were sequenced using a thermal asymmetric interlaced-PCR (TAIL-PCR) method. This region contains 10 potential Sp1 binding sites and lacks a TATA box. Rapid amplification of cDNA ends (RACE) revealed the transcriptional start site at -14 bp. A CA/GT microsatellite repeat was identified with a hybridization-based method and was converted to a sequence-tagged site (STS). The GT microsatellite repeat was localized to intron 2 approximately 150 bp downstream of the exon-intron junction. Two alleles, (GT)10 and (GT)11, were detected in both EH patients and age-matched normotensive (NT) controls. Multiple logistic linear regression analysis indicated that the NPR-B genotype is associated significantly with EH (odds ratio 1.55; 95% confidence interval, 1.02 to 2.35). The (GT)11 frequency was 0.316 (65/206) for the EH group and 0.218 (44/202) for the NT group and differed significantly between the EH and NT groups (chi2=4.97, P=0.026). The structural organization of the human NPR-B gene was determined, and a novel GT repeat polymorphism, which associated with EH, was identified. These results suggest that one cause of EH is a mutation in this gene or a closely related gene or region.

Base Sequence↗
PubMed1999

Clinical utility of negative contrast intravascular ultrasound to evaluate plaque morphology before and after coronary interventions.

Although intravascular ultrasound (IVUS) is used for evaluation of plaque volume and lumen size as well as detection of vessel wall structures after catheter-based interventions, differentiation between the lumen and plaque structures can be difficult. This study attempted to evaluate the efficacy of negative contrast IVUS imaging for assessment of vessel wall morphology after coronary interventions. IVUS studies were performed in 67 lesions in 66 patients before and after coronary interventions. After the baseline ultrasound imaging run, warm 5% glucose solution was injected manually through the guiding catheter into the coronary artery to washout blood from the lumen to avoid speckled reflections from red blood cells (negative contrast). Quantitative measurements were obtained and plaque morphology was assessed for the presence and extent of medial dissections and intimal flaps. There was no difference in each quantitative parameter between baseline images and negative contrast images. The vessel wall boundary was clearly delineated from the lumen, which was defined as effective negative contrast in 51 of 67 lesions (76%). The baseline images revealed plaque dissection in 9 lesions (18%) and an intimal flap in 13 lesions (25%). In addition, 4 dissections (8%) and 16 intimal flaps (31%) were visualized during the infusion of negative contrast. Additional treatment was performed in 4 lesions (8%) based on the images with negative contrast. Negative contrast IVUS was more sensitive in demonstrating a plaque fracture than were baseline images. This method is useful for enhancing the diagnostic capability of IVUS imaging and may influence the decision-making process during interventional procedures.

Anatomy, Cross-Sectional↗
PubMed1999

The role of sialidase in the development of hypocomplementemia in postinfectious acute glomerulonephritis.

The role of sialidase in complement activation and in development of hypocomplementemia in patients with postinfectious acute glomerulonephritis (AGN) was investigated. In sera from 17 patients with AGN and 14 healthy controls, sialidase activity and serum levels of free and total sialic acid were measured by previously established methods. Circulating sialidase activity and serum levels of free and total sialic acid and haptoglobin were increased, and the C3 level was decreased in the acute phase of AGN. There was no correlation between free sialic acid and total sialic acid, which increased in parallel with serum levels of haptoglobin, one of the acute-phase reactants. A follow-up study of these parameters in a typical case reflected this tendency and suggested that increased sialidase after infection, in addition to complement activation by the infectious substance, could play a role in development of hypocomplementemia. To clarify this mechanism, purified neuraminidase was incubated with normal human serum under various conditions. Complement breakdown products were measured in the incubation mixture by enzyme-linked immunosorbent assay using monoclonal antibodies against iC3b, Bb, and C4d neoantigens. iC3b was generated dose-dependently in the presence of neuraminidase. Further examination revealed that iC3b and Bb were generated in the incubation mixture with neuraminidase and NHS and that C4d was not detected in the same mixture. These findings indicate that neuraminidase activates the alternative complement pathway. These in vitro data, together with the former in vivo data led us to conclude that increased sialidase after infection could accelerate the complement amplification system, resulting in hypocomplementemia in the acute phase of postinfectious AGN.

Acute Disease↗
PubMed1999

Evidence for the delayed effect in human ischemic preconditioning: prospective multicenter study for preconditioning in acute myocardial infarction.

OBJECTIVES: This study aimed to investigate prospectively the protective effect of a first preinfarction angina attack against acute myocardial infarction (AMI) in human hearts without significant collaterals. BACKGROUND: Several retrospective studies and the prospective studies have demonstrated the existence of the preconditioning (PC) effect in humans. However, collaterals were not examined in the prospective studies. In animal models, the PC effect on myocardial infarct size appears soon after PC reperfusion (classic) but disappears within 1 to 2 h. It then reappears 24 to 48 h after reperfusion (the delayed PC effect). Meanwhile, the PC effect on stunning appears 12 h after PC reperfusion (the delayed PC effect). The concept of the classic and delayed PC effects has not been investigated in human AMI studies. If the above concept is also correct in humans, the infarct size and/or impairment of the left ventricular function should be inversely correlated with the time interval between the first preinfarction angina attack and the onset of AMI when that time interval is limited to between 2 and 48 h. METHODS: The subjects were 25 patients with first AMI of the proximal left anterior descending artery who underwent successful direct percutaneous transluminal coronary angioplasty (PTCA) 2 to 6 h after the onset and with no (or poor) collateral circulation (grade 0 or 1). They were divided into two groups: preinfarction angina (PA)(+) group: 11 patients with new onset preinfarction angina from 2 to 48 h before the onset, PA(-) group: 14 patients without angina before infarction. Peak creatine kinase (CK) and cumulative CK were examined, and the left ventricular ejection fraction (LVEF) and the regional wall motion (RWM) were determined from the left ventriculograms during the acute (immediately after the coronary reperfusion) and chronic (four weeks after the onset of AMI) phases. The RWM index (RWMI) was then calculated as the mean motion of chords (standard deviation [SD]/chord) lying in the area of chords of RWM < or = -2 SD in the acute phase (ischemic risk area). RESULTS The increase in the RWMI between the acute and chronic phases was significantly larger in the PA(+) group than in the PA(-) group (1.55 +/- 1.32 and 0.69 +/- 0.75, p < 0.05, respectively) although no significant difference in the enzymatic infarct size was seen between the two groups. The increases in the LVEF and the RWMI were significantly correlated with the time interval from the first preinfarction angina attack to the onset of AMI (r = 0.622, p < 0.05 and r = 0.646, p < 0.05, respectively), but the enzymatic infarct size was not. CONCLUSIONS: The beneficial effect of preinfarction angina on left ventricular wall motion, independently of collateral flows, indicates the existence of the PC effect in humans. The greater protective effect of a longer time interval between angina pectoris and AMI suggests that the protection is due to a delayed PC effect.

Angina Pectoris↗
PubMed1999

Nucleotide sequence of the 5'-flanking region of the type A human natriuretic peptide receptor gene and association analysis using a novel microsatellite in essential hypertension.

We isolated the 5'-flanking region of the type A human natriuretic peptide receptor gene (hNPRA) using thermal asymmetric interlaced polymerase chain reaction (TAIL-PCR). The 2.1-kb 5' sequence upstream of the hNPRA gene lacks a TATA box but contains three potential Sp1-binding sites and an inverted CCAAT box. Moreover, we discovered a novel dinucleotide repeat marker approximately 300 bp upstream of the start codon. Using this microsatellite marker, we performed an association study in patients with essential hypertension (EH). One hundred twenty-five patients with essential hypertension and 125 age-matched subjects with normal blood pressure were studied. The number of TC/GA repeats of the three alleles ranged from 10 to 12 repeats in the 250 unrelated Japanese subjects. The allele frequency distribution in the two groups were not significantly different. Thus, the microsatellite polymorphism in the hNPRA gene is not associated with EH.

Base Sequence↗
PubMed1999

Increased IL-12 release by monocytes in nephrotic patients.

The pathogenesis of minimal-change nephrotic syndrome (MCNS) is obscure. It has been postulated that this glomerular disease may be a systemic disorder of cell-mediated immunity. IL-12 is a heterodimeric cytokine that is produced primarily by antigen-presenting cells and plays a primary role in the induction of cell-mediated immunity. To gain insight into the involvement of this cytokine, in vitro IL-12 levels were assessed in patients with MCNS and IgA nephropathy (IgAN) who were in either a stable or active clinical condition. The levels were compared with values in healthy controls. Significantly increased spontaneous and lipopolysaccharide (LPS)-stimulated release of IL-12 was detected in peripheral blood monocyte (PBM) cultures of MCNS and IgAN patients with the nephrotic syndrome (NS) compared with those of normal controls. Moreover, when individual MCNS patients were followed through their clinical illness, IL-12 levels were increased during the active phase and normalized as the patients went into remission. The amounts of IL-12 are significantly correlated with the levels of vascular permeability factor (VPF) in MCNS patients. This study describes a correlation between in vitro IL-12 release by PBM from two types of nephrotic patients and their disease activity, as well as a correlation with release of VPF by the same cultures. The study contributes to the understanding of this class of diseases and the observations may have a prognostic/diagnostic value.

Adult↗
PubMed1999

Contribution of synthetic phenotype on the enhanced angiotensin II-generating system in vascular smooth muscle cells from spontaneously hypertensive rats.

OBJECTIVE: We have demonstrated that cultured vascular smooth muscle cells (VSMC) from spontaneously hypertensive rats (SHR), but not from normotensive Wistar-Kyoto (WKY) rats, produce angiotensin II (Ang II) in a homogeneous culture with increased levels of angiotensinogen, cathepsin D and angiotensin converting enzyme (ACE) at early passages. In the current study, we investigated how changes in the cell phenotype affect the Ang II-generating system and the growth of VSMC from SHR. DESIGN AND METHODS: We evaluated basal DNA synthesis by [3H]thymidine incorporation, immunofluorescence of alpha-smooth muscle (SM) actin, mRNA expression of phenotype markers such as SM22alpha appeared by contractile phenotype, Ang II-generating system components and growth factors by reverse transcription and polymerase chain reaction analysis, and Ang II levels by radioimmunoassay in quiescent VSMC from WKY/Izumo rats and SHR/Izumo at passages 4, 8 and 12. RESULTS: Basal DNA synthesis in VSMC from WKY rats increased with increasing passage number, whereas in cells from SHR it was markedly higher at early passages and was not affected by the passages. At early passage numbers, immunofluorescence of alpha-SM actin was stronger in VSMC from WKY rats than in cells from SHR, but decreased after several passages. Expression of SM22alpha mRNA was higher in VSMC from WKY rats than in cells from SHR at early passages, and decreased after several passages in cells from both rat strains. Expression of matrix Gla mRNA was higher in VSMC from SHR than in cells from WKY rats at early passage, and increased after several passages in cells from both rat strains. Ang II was not detected at early passages but increased in VSMC from WKY rats with increasing passage, whereas it was detected in VSMC from SHR at early passages and did not change with the passages. Expression of angiotensinogen mRNA was higher in VSMC from SHR than in cells from WKY rats, and was not affected by the passages. Expressions of cathepsin D and ACE mRNA were higher in VSMC from SHR than in cells from WKY rats at early passage, and were increased by the passages in VSMC from WKY rats. Expressions of transforming growth factor-beta1, platelet-derived growth factor A-chain, and basic fibroblast growth factor mRNA were significantly higher in VSMC from SHR than in cells from WKY rats, and were increased by the passages. CONCLUSION: These data indicate that early in culture VSMC from SHR have the synthetic phenotype, whereas VSMC from WKY rats have the contractile phenotype which then changes to the synthetic phenotype after increased passage numbers, with increased expression of cathepsin D and ACE, which produce Ang II, and increased expression of Ang II-related growth factors, which induce the exaggerated growth observed in VSMC from SHR.

Angiotensin II↗
PubMed1999

Low dose of eicosapentaenoic acid inhibits the exaggerated growth of vascular smooth muscle cells from spontaneously hypertensive rats through suppression of transforming growth factor-beta.

OBJECTIVE: To evaluate effects of eicosapentaenoic acid (EPA), an n-3 polyunsaturated fatty acid, on the exaggerated growth of vascular smooth muscle cells (VSMC) from spontaneously hypertensive rats (SHR). DESIGN: Cultured VSMC were prepared by an explant method from thoracic aortas in 8-week-old male Wistar-Kyoto (WKY)/Izumo rats and SHR/Izumo. Effects of EPA on basal DNA synthesis, expression of growth factors and cyclin-dependent kinase 2 (cdk2) activity were examined in VSMC from WKY rats and SHR. METHODS: The cell cycles were synchronized with serum deprivation, then DNA synthesis in VSMC was measured by [3H]-thymidine incorporation. Fatty acid composition of the phospholipid fraction in VSMC was measured by gas chromatography. Expression of platelet-derived growth factor (PDGF) A-chain, transforming growth factor (TGF)-beta1 and basic fibroblast growth factor (bFGF) mRNAs was evaluated by reverse-transcription and polymerase chain reaction analysis. Cdk2 activity was determined by autoradiography after polyacrylamide gel electrophoresis of VSMC extracts that had been immunoprecipitated with anti-cdk2 antibody and protein A sepharose, and then incubated with 32P-ATP and histone H1. RESULTS: High concentrations (40 and 80 micromol/I) of EPA significantly inhibited basal DNA synthesis in VSMC from both rat strains. Low dose (20 micromol/l) of EPA significantly inhibited basal DNA synthesis in VSMC from SHR, whereas the same dose of EPA stimulated DNA synthesis in VSMC from WKY rats. In analysis of fatty acid composition, low dose of EPA was considerably incorporated in VSMC. Low dose of EPA significantly inhibited angiotensin II- and phorbol ester milisterol-stimulated DNA synthesis in VSMC from both rat strains, whereas EPA did not affect PDGF-AA-stimulated DNA synthesis in VSMC from either rat strain. Low dose of other polyunsaturated fatty acids such as docosahexaenoic acid, arachidonic acid and linoleic acid did not significantly affect basal DNA synthesis in VSMC from either strain. Low dose of EPA significantly inhibited expression of TGF-beta1 mRNA in VSMC from SHR, whereas EPA did not affect expression of PDGF A-chain and bFGF mRNAs in VSMC from SHR. Cdk2 activity in VSMC from SHR was higher than that from WKY rats. Low dose of EPA inhibited cdk2 activity in VSMC from SHR, whereas it stimulated the activity in VSMC from WKY rats. CONCLUSION: Low dose of EPA exerted specific inhibition of the exaggerated growth of VSMC from SHR through the suppression of TGF-beta.

Animals↗
PubMed1999

Nitric oxide synthase gene polymorphism and its influence on cardiovascular disease.

Several lines of evidence indicate a significant association between variations of the endothelial constitutive nitric oxide synthase gene and the incidence of cardiovascular disease, and discrepant findings may be attributable to racial differences. The detection of functional allelic polymorphisms may be needed to confirm this association, because direct evidence to support a causative role for the endothelial constitutive nitric oxide synthase gene is not yet available. There are no available data to confirm that neural and inducible nitric oxide synthases are associated with cardiovascular diseases.

Cardiovascular Diseases↗
PubMed1999

Interleukin-4 cooperates with interleukin-10 to inhibit vascular permeability factor release by peripheral blood mononuclear cells from patients with minimal-change nephrotic syndrome.

Increased production of a vascular permeability factor (VPF) from peripheral blood mononuclear cells (PBMC) in patients with minimal-change nephrotic syndrome (MCNS) has been reported. Interleukin-4 (IL-4) and interleukin-10 (IL-10), both produced by T-helper type-2 cells, are cytokines with the capacity to downregulate proinflammatory responses. To gain insight into the immunoregulatory properties of these cytokines, we analyzed the effects of recombinant human IL-4 and IL-10 on VPF release in MCNS patients. In the present study we show that the regulatory cytokines IL-4 and IL-10 are potent inhibitors of the VPF activity of concanavalin A-activated MCNS PBMC. Each cytokine was found to suppress VPF release in a dose-dependent manner. Moreover, when used at suboptimal concentrations, a combination of the two cytokines resulted in enhanced suppression of VPF release. Neutralization of endogenously produced IL-4 and IL-10 by both anti-IL-4 and anti-IL-10 antibodies resulted in an increased release of VPF. These data demonstrate that IL-4 acts in concert with IL-10 to inhibit VPF release and suggest that they are effective biologic regulators of the VPF responses in vitro.

Adolescent↗
PubMed1999

Complement activation accelerates glomerular injury in diabetic rats.

A known inhibitor of the complement cascade (K-76 COONa) was administered to an inbred diabetic rat model to investigate whether the complement system may play a role in the progression of diabetic glomerulosclerosis. Drinking water containing K-76 COONa was available continuously to inbred diabetic rats (Otsuka Long-Evans Tokushima Fatty, OLETF) from the age of 25 to 55 weeks (Group L). Drinking water without K-76 COONa was similarly available to OLETF rats (Group H) and nondiabetic control rats (Long-Evans Tokushima Otsuka, LETO) (Group C). The levels of plasma glucose (mg/dl) at the 55th week were 156 +/- 16 in Group C, 252 +/- 18 in Group L and 349 +/- 93 in Group H. There was no significant difference in the degree of diabetes between Group L and Group H. The levels of urinary protein at 55 weeks of age (mg/day) were 2.1 +/- 0.4 in Group C, 11. 6 +/- 1.5 in Group L and 18.0 +/- 2.8 in Group H. The level of urinary protein was significantly decreased by the administration of K-76 COONa. Histological examination of renal specimens from the sacrificed rats at 55 weeks of age revealed diffuse mesangial expansion in almost all glomeruli in Group H, exudative lesions in 30% of glomeruli in Group H, and only mild mesangial expansion was recognized in Group L. Immunofluorescence study revealed brilliant staining of C3 and immunoglobulins (Ig) in Group H; trace staining of Ig and no staining of C3 were recognized in Group L. The incubation study with guinea pig serum and glomeruli from rats revealed that Ig and complement components also bound to injured glomeruli in vitro. These data indicate that the complement cascade is activated by injured glomeruli and this activation exacerbates diabetic glomerulosclerosis.

Animals↗
PubMed1999

Effects of interleukin-15 on vascular permeability factor release by peripheral blood mononuclear cells in normal subjects and in patients with minimal-change nephrotic syndrome.

The characteristic function of interleukin (IL)-15 appears to be its ability to mimic the stimulatory action of IL-2 on lymphocytes by utilizing part of the IL-2 receptor complex. To gain insight into the immunoregulatory properties of this cytokine in patients with minimal-change nephrotic syndrome (MCNS), we analyzed effects of IL-15 on vascular permeability factor (VPF) release in vitro. Peripheral blood mononuclear cells (PBMC) were isolated from 16 patients with MCNS, 16 patients with IgA nephropathy (IgAN) and 16 healthy controls. Cells were stimulated with concanavalin A (Con A) and the VPF was assessed using the method of Lagrue with minor modifications. PBMC secreted significantly increased amounts of VPF under stimulation with Con A in patients with MCNS and IgAN patients with the nephrotic syndrome as compared with normal controls. Here we have demonstrated, for the first time, that addition of IL-15 to PBMC obtained from nephrotic patients as well as from normal controls increased Con A-induced release of VPF by 250%. This stimulatory effect was found highly significant and was dose-dependent. The effect of IL-15 on the secretion of VPF was specific, since a complete reversion was obtained with a neutralizing antibody to human IL-15. Our findings reveal that IL-15 has the potential to function as an immunoregulatory molecule of PBMC VPF release. In addition, IL-15 had similar effects to IL-2 in terms of its capacity to upregulate VPF release. Taken together, our data emphasize a positive regulatory role for IL-15 in inducing the release of VPF when present at optimal levels. Therefore, IL-15 antagonists may provide a basis for immune intervention in the pathophysiology of VPF.

Adult↗
PubMed1999

Production of angiotensin II by homogeneous cultures of vascular smooth muscle cells from spontaneously hypertensive rats.

Production of angiotensin II (Ang II) in spontaneously hypertensive rats (SHR)-derived vascular smooth muscle cells (VSMC) has now been investigated. A nonpeptide antagonist (CV-11974) of Ang II type 1 receptors inhibited basal DNA synthesis in VSMC from SHR, but it had no effect on cells from Wistar-Kyoto (WKY) rats. Ang II-like immunoreactivity, determined by radioimmunoassay after HPLC, was readily detected in conditioned medium and extracts of SHR-derived VSMC, whereas it was virtually undetectable in VSMC from WKY rats. Isoproterenol increased the amount of Ang II-like immunoreactivity in conditioned medium and extracts of SHR-derived VSMC, whereas the angiotensin-converting enzyme inhibitor delapril significantly reduced the amount of Ang II-like immunoreactivity in conditioned medium and extracts of these cells. Reverse transcription-polymerase chain reaction analysis revealed that the abundance of mRNAs encoding angiotensinogen, cathepsin D, and angiotensin-converting enzyme was greater in VSMC from SHR than in cells from WKY rats. The abundance of cathepsin D protein by Western blotting was greater in VSMC from SHR than in cells from WKY rats. Ang I-generating and acid protease activities were detected in VSMC from SHR, but not in cells from WKY rats. These results suggest that SHR-derived VSMC generate Ang II with increases in angiotensinogen, cathepsin D, and angiotensin-converting enzyme, which contribute to the basal growth. Production of Ang II by homogeneous cultures of VSMC is considered as a new mechanism of hypertensive vascular disease.

Angiotensin II↗
PubMed1999

Radiofrequency catheter ablation of coexistent atrioventricular reciprocating tachycardia and left ventricular tachycardia originating in the left anterior fascicle.

Coexistence of supraventricular tachycardia and ventricular tachycardia is rare. A patient with no structural heart disease and wide QRS complex tachycardia with a right bundle block configuration and right-axis deviation underwent electrophysiological examination. A concealed left atrioventricular pathway (AP) was found, and atrioventricular reciprocating tachycardia (AVRT) and left ventricular tachycardia (VT) originating in or close to the anterior fascicle of the left ventricle were both induced. Radiofrequency (RF) catheter ablation of the concealed left AP was successfully performed. Ten months later, VT recurred and was successfully ablated using a local Purkinje potential as a guide. Coexistent AVRT and idiopathic VT originating from within or near the left anterior fascicle were successfully ablated.

Adult↗
PubMed1999

Effect of insulin resistance on the endothelial vasomotor function of the coronary artery of nondiabetic patients.

Attention has been paid to the relationship between insulin resistance and coronary artery disease. The present study investigated the relationship between insulin resistance and the endothelial vasomotor function of the coronary artery of nondiabetic patients with chest pain and a positive exercise tolerance test. Twenty-five nondiabetic patients with chest pain were included. Patients with a steady state plasma glucose (SSPG) level of greater than or equal to 135 mg/dl were placed in the insulin resistant (IR) group, and those with a SSPG level less than 135 mg/dl were placed in the noninsulin resistant (NIR) group. The effect of acetylcholine, papaverine, and isosorbide dinitrate on the vasomotor response of the coronary endothelium was studied. The percent change in diameter of the coronary artery after injection of acetylcholine (20 microg ml(-1) min(-1)) was 84+/-17% in the IR group, and 109+/-18% in the NIR group. The difference in the degree of the vasodilative response is statistically significant (p<0.01). The percent change in coronary flow velocity after injection of acetylcholine (20 microg ml(-1) min(-1)) in the IR group was 120+/-67%, whereas that in the NIR group was 256+/-58%; the increase in coronary artery flow velocity of the IR group was significantly smaller than that of the NIR group (p<0.01). Nondiabetic patients with insulin resistance have endothelial vasomotor dysfunction, which raises an important question as to whether nondiabetic patients with insulin resistance should be treated to prevent the development of coronary heart disease.

Acetylcholine↗
PubMed1999

Effects of combined emergency percutaneous cardiopulmonary support and reperfusion treatment in patients with refractory ventricular fibrillation complicating acute myocardial infarction.

OBJECT: We conducted a prospective study to determine whether or not combined emergency percutaneous cardiopulmonary support (PCPS) and coronary reperfusion treatment are useful for acute myocardial infarction (MI) patients with unsynchronized electric shock-resistive ventricular fibrillation (VF). PATIENTS AND METHODS: Thirty-two acute MI patients who lapsed into the refractory VF were entered into the study. Group 1 consisted of 19 patients with VF outside the hospital, and Group 2 consisted of 13 patients with VF immediately after arrival at the hospital. The primary endpoint was successful reperfusion, return of spontaneous circulation and good recovery without neurologic disability. RESULTS: The infarct-related arteries showed a significant difference between Groups 1 and 2. However, the two groups had similar rates of successful reperfusion (84.6% vs 94.7%, respectively) and return of spontaneous circulation (89.5% vs 84.6%, respectively). The rates of good recovery were similarly low in both groups (5.3% vs 15.4%, respectively). CONCLUSION: Combined emergency PCPS and reperfusion treatment produced high return of spontaneous circulation, however the neurologic outcome was low.

Assisted Circulation↗