Structure and function of AQP2.
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Animals↗
Biomedical subjects
F Marumo
Publications and source records attributed to F Marumo.
Clinical significance of residual slow cavotricuspid isthmus conduction after ablation of typical atrial flutter.
The purpose of this study was to evaluate the clinical significance of residual slow cavotricuspid isthmus (IT) conduction on the ablation line after typical atrial flutter (AF) ablation, undetected by analysis of right atrial (RA) activation. Seventy patients with AF underwent IT ablation. In the first 35 patients (group I), IT block was verified only by the RA activation sequence. In the subsequent 35 patients (group II), IT block was verified by the presence of parallel double potentials with an isoelectric interval through the entire ablation line (in addition to RA activation sequence criteria) during pacing from the low lateral RA and the coronary sinus ostium. In group I patients, residual IT conduction was retrospectively analyzed at the ablation site immediately after the last radiofrequency (RF) application. Six of 33 group I patients (18%) with IT block had residual IT conduction represented by fractionated or multicomponent potentials immediately after the final RF application. Four of these 6 patients (67%) had recurrences of AF, 3 +/- 1.4 months after ablation. Four (12%) of 33 group II patients with IT block had residual IT conduction in the ablation line after creation of IT block confirmed by RA activation sequence. This conduction was eliminated by 1.6 +/- 0.9 further RF applications in all 4 patients. No AF recurrence was observed in group II patients. Up to 18% of patients with apparent IT ablation had residual slow IT conduction on the ablation line. This conduction was associated with AF recurrences and must be eliminated to achieve complete cure of AF.
Aged↗
Nonlinear ablation targeting an isthmus of critically slow conduction detected by high-density electroanatomical mapping for atypical atrial flutter.
Focused high-density atrial endocardial mapping was performed with a three-dimensional electroanatomical mapping system or a multielectrode basket catheter in six men and two women (mean age = 54 years) with atypical atrial flutter (AFL) to characterize its reentry circuit and identify its isthmus of critically slow conduction (ICSC). Activation mapping revealed figure-8 reentry with ICSC between a surgical atrial scars in three atypical AFLs following atriotomy, and between the crista terminalis (CT) and the inferior (IVC) or superior (SVC) vena cavae in atypical right atrial (RA) AFL in absence of prior atriotomy. Figure-8 double loop reentry was documented in one RA atypical AFL. ICSC was characterized by concealed entrainment with a post-pacing interval identical to the AFL cycle length, and a mid-diastolic fractionated electrogram, 129 +/- 23 ms in duration, spanning the isoelectric line between double potentials on adjacent area of conduction block. All AFLs were successfully ablated with 4.9 +/- 4.3 RF pulses applied at ICSC. A possible mechanism of atypical AFL consists of figure-8 reentry with ICSC between surgical scars in postoperative AFL, and between the CT and the IVC/SVC in RA AFL not preceded by cardiac surgery. Late and partial regeneration of conduction across the atriotomy scar can create an ICSC. Nonlinear ablation targeting ICSC can cure atypical AFL, whether it follows surgery or not.
Atrial Flutter↗
Electrocardiographic characteristics of left ventricular outflow tract tachycardia.
Catheter ablation of idiopathic left ventricular outflow tract tachycardia (LVOT-VT) is rare because a safe ablation technique at this site has not been described, and serious complications may occur. This study compared the QRS morphology of LVOT-VT with that of idiopathic right ventricular outflow tract tachycardia. A comparison was made between the electrocardiographic characteristics of LVOT-VT originating from the supravalvular region of a coronary cusp (Supra-Ao group) with those of LVOT-VT originating from the infravalvular endocardial region of a coronary cusp of the aortic valve within the LV (Infra-Ao group). After precise mapping of the right ventricle, left ventricle, pulmonary artery, coronary cusps, and proximal portion of the anterior interventricular vein, there were 17 patients in whom VT was thought to be located at the LVOT by both activation and pace mapping. They were divided between a Supra-Ao group (n = 8), and an Infra-Ao group (n = 9). Analysis of the 12-lead electrocardiogram (ECG) revealed an S wave in lead I in all 17 patients. A precordial R wave transition was also observed at V1 or V2 in 16 patients (94%). In 7 of 8 patients (88%) with Supra-Ao LVOT-VT, no S wave was observed in either V5 or V6. In contrast, an Rs pattern was observed in both V5 and V6, or in V6 only, in 100% of the patients with Infra-Ao LVOT-VT. A LVOT-VT should be suspected when the ECG shows an S wave in lead I and an R/S ratio greater than 1 in lead V1 or V2, versus a coronary cusp location if there is no S wave in either lead V5 or V6.
Adolescent↗
Transcriptional regulation of the CLC-K1 promoter by myc-associated zinc finger protein and kidney-enriched Krüppel-like factor, a novel zinc finger repressor.
The expression of CLC-K1 and CLC-K2, two kidney-specific CLC chloride channels, is transcriptionally regulated on a tissue-specific basis. Previous studies have shown that a GA element near their transcriptional start sites is important for basal and cell-specific activities of the CLC-K1 and CLC-K2 gene promoters. To identify the GA-binding proteins, the human kidney cDNA library was screened by a yeast one-hybrid system. A novel member of the Cys2-His2 zinc finger gene designated KKLF (for "kidney-enriched Krüppel-like factor") and the previously isolated MAZ (for "myc-associated zinc finger protein") were cloned. KKLF was found to be abundantly expressed in the liver, kidneys, heart, and skeletal muscle, and immunohistochemistry revealed the nuclear localization of KKLF protein in interstitial cells in heart and skeletal muscle, stellate cells, and fibroblasts in the liver. In the kidneys, KKLF protein was localized in interstitial cells, mesangial cells, and nephron segments, where CLC-K1 and CLC-K2 were not expressed. A gel mobility shift assay revealed sequence-specific binding of recombinant KKLF and MAZ proteins to the CLC-K1 GA element, and the fine-mutation assay clarified that the consensus sequence for the KKLF binding site was GGGGNGGNG. In a transient-transfection experiment, MAZ had a strong activating effect on transcription of the CLC-K1-luciferase reporter gene. On the other hand, KKLF coexpression with MAZ appeared to block the activating effect of MAZ. These results suggest that a novel set of zinc finger proteins may help regulate the strict tissue- and nephron segment-specific expression of the CLC-K1 and CLC-K2 channel genes through their GA cis element.
Amino Acid Sequence↗
Mechanical stretch stimulates growth of vascular smooth muscle cells via epidermal growth factor receptor.
We have studied whether activation of epidermal growth factor receptor (EGFR) is involved in stretch-induced extracellular signal-regulated kinase 1/2 (ERK1/2) activation and protein synthesis in cultured rat vascular smooth muscle cells (VSMC). Cyclic stretch (1 Hz) induced a rapid (within 5 min) phosphorylation of ERK1/2, an effect that was time and strength dependent and inhibited by an EGFR kinase inhibitor (AG-1478) but not by a platelet-derived growth factor receptor kinase inhibitor (AG-1296). The stretch rapidly (within 2 min) induced tyrosine phosphorylation of several proteins, among which 180-kDa protein was shown to be EGFR as revealed by blockade with AG-1478 as well as immunoprecipitation with anti-EGFR antibody coupled with immunoblotting with anti-phosphotyrosine antibody. The stretch rapidly (within 2 min) induced association of tyrosine-phosphorylated EGFR with adaptor proteins (Shc/Grb2) as revealed by coprecipitation with glutathione-S-transferase-Grb2 fusion protein coupled with immunoblotting with anti-phosphotyrosine, anti-EGFR, and anti-Shc antibodies. Transfection of a dominant-negative mutant of H-Ras also inhibited stretch-induced ERK1/2 activation. Treatment with a stretch-activated ion channel blocker (Gd(3+)) and an intracellular Ca(2+) antagonist (TMB-8) inhibited stretch-induced phosphorylation of EGFR and ERK1/2. Treatment with AG-1478 and a mitogen-activated protein kinase kinase inhibitor (PD-98059), but not AG-1296, blocked [(3)H]leucine uptake stimulated by a high level of stretch. These data suggest that ERK1/2 activation by mechanical stretch requires Ca(2+)-sensitive EGFR activation mainly via stretch-activated ion channels, thereby leading to VSMC growth.
Adaptor Proteins, Signal Transducing↗
Mutations in sixth transmembrane domain of AQP2 inhibit its translocation induced by vasopression.
Vasopression-induced phosphorylation of serine 256 of the aquaporin-2 (AQP2) water channel triggers translocation of the protein from cystolic reservoir vesicles to the apical membrane of collecting duct principal cells. Dileucine motifs are located in the sixth transmembrane domain (6TM) of AQP2 and are known as the signal sequence for internalization, sorting from the trans-Golgi network to endosomes/lysosomes, and basolateral sorting. In this study, involvement of 6TM in vasopressin-induced translocation of the protein was investigated. A series of mutations in 6TM of AQP2 was introduced to rat cDNA and expressed in LLC-PK(1) cells. Immunofluorescence microscopy indicated that the mutant AQP2 proteins were retained in the cytoplasm after vasopressin stimulation, which actually promoted the plasma membrane expression of wild-type protein. Immunoelectron microscopy showed that the mutant AQP2 proteins reached the endosomes but did not reach the plasma membrane. These results demonstrate that 6TM has essential domains for vasopressin-induced translocation from endosomes to the plasma membrane.
Animals↗
Analysis of urea nitrogen and creatinine kinetics in hemodialysis: comparison of a variable-volume two-compartment model with a regional blood flow model and investigation of an appropriate solute kinetics model for clinical application.
To investigate an appropriate solute kinetics model for clinical application, we analyzed urea nitrogen (UN) and creatinine (Cr) kinetics by a variable-volume two-compartmental model (2CM) and a regional blood flow model (RBF) in 44 hemodialysis patients with varying proportions of first compartmental volume and regional volume (p(1)). Solute kinetics could not be solved in some of the patients with higher p(1) values, and there were more solution failures by the RBF than by the 2CM. The solute generation rate (g) and solute distribution volume in the dry state (V(D)) increased with increases in p(1) in both models, but there were some differences between the two models. When g was normalized by V(D), it became relatively constant, irrespective of the p(1) value or model used (0.133 +/- 0.029 mg/min/l by the 2CM and 0.132 +/- 0.029 mg/min/l by the RBF for UN; 0.0200 +/- 0.0049 mg/min/l by the 2CM and 0.0198 +/- 0.0048 mg/min/l by the RBF for Cr). The intercompartmental mass transfer coefficient (K(c); liters/min) calculated by the 2CM decreased as p(1) increased (K(c) = -1.77.p(1) + 1.16, p < 0.0001, R = 0.999 for UN; K(c) = -0.847.p(1) + 0.556, p < 0.0001, R = 1.000 for Cr). The systemic blood flow (Q(sys); liters/min) calculated by the RBF also decreased as p(1) increased (Q(sys) = -11.1.p(1) + 6.21, p < 0.0005, R = 1.000 for UN; Q(sys) = -5.22.p(1) + 2.90, p < 0.001, R = 0.999 for Cr). Since the RBF more frequently failed to solve the solute kinetics and since there was a difference in its Q(sys) values for UN and Cr, the 2CM was considered to be a superior model. When p(1) was extremely low, the 2CM could be transformed into a modified variable-volume one-compartment model (1CM) which presented a similar g/V(D) (0.133 +/- 0.029 for UN; 0.0200 +/- 0.0048 for Cr). This modified 1CM was considered to satisfy appropriate conditions for clinical application, since it is simpler than the 2CM and provides useful information on the dialysis dose.
Aged↗
Endothelin-1 inhibits apoptosis of vascular smooth muscle cells induced by nitric oxide and serum deprivation via MAP kinase pathway.
Endothelin (ET)-1, an endothelium-derived vasoconstrictor and mitogen, acts as an antiapoptotic factor against serum deprivation-induced apoptosis of endothelial cells and fibroblasts but enhances apoptosis of some cancer cells. In the present study, we examined whether nitric oxide (NO) and ET-1 modulate apoptosis of rat vascular smooth muscle cells (VSMCs) via the mitogen-activated protein (MAP) kinase pathway. Both serum deprivation and NO donors (FK409 and SNAP) caused apoptosis of VSMCs, as demonstrated by TdT-mediated dUTP-biotin nick end-labeling, appearance of fragmented DNA, and induction of caspase-3 activity. ET-1 dose-dependently antagonized apoptosis induced by serum deprivation and NO donors. A selective ET(A) receptor antagonist (BQ123) and a nonselective ET(A/B) receptor antagonist (TAK044), but not a selective ET(B) receptor antagonist (BQ788), inhibited the antiapoptotic effect of ET-1, indicating that the antiapoptotic effect of ET-1 is mediated via the ET(A) receptor. ET-1 activated MAP kinase, whose effect was inhibited by FK409. Transfection with an unphosphorylated wild-type MAP kinase kinase-1 (MAPKK-1) or its constitutively activated mutant protected VSMCs against apoptosis induced by serum deprivation and NO donors. Inhibition of MAP kinase activity with PD98059, a specific inhibitor of MAPKK-1, or by transfection of a dominant-negative MAPKK-1 mutant antagonized the antiapoptotic effect of ET-1, suggesting the involvement of MAP kinase in the antiapoptotic effect. The potent inhibitory effect of ET-1 on apoptosis of VSMCs induced by serum deprivation and NO suggests that the counterbalance between the 2 endothelium-derived factors contributes to the process of vascular remodeling by determining VSMC survival and death, respectively, via a common MAP kinase pathway.
Animals↗
Effects of 'cool-down' during exercise recovery on cardiopulmonary systems in patients with coronary artery disease.
The effects of 'cool-down' during exercise recovery on cardiovascular and respiratory systems have not been fully clarified. The recovery of respiratory gasses was compared in cardiac patients after maximal exercise during which subjects either performed a cool-down or rested. Twenty-one patients (61+/-10 years) with coronary artery disease performed 2 symptom-limited incremental exercise tests on a cycle ergometer: one with a cool-down and the other without during recovery from the maximal exercise test. Expired gasses were analyzed on a breath-by-breath basis throughout the test and for 6min of recovery. Without a cool-down, the ventilatory equivalent for O2 (VE/O2) increased dramatically during recovery compared with the resting values or those of peak exercise: 44.5+/-7.7 at rest, 44.0+/-10.6 at peak exercise and 63.3+/-14.5 after 2min of recovery. End-tidal PO2 (P(ET)O2) also increased significantly during recovery. However, the overshoot phenomenon of these variables was attenuated when cool-down exercise was performed during recovery. The high ratio of VE/VO2 reflects ventilation perfusion (VA/Q) unevenness and P(ET)O2 is an index of arterial PO2. Thus, it is suggested that cool-down exercise during recovery after maximal exercise testing provides beneficial effects on the respiratory system by decreasing the VA/Q unevenness and relative hyperventilation that are observed when cool-down exercise is not performed.
Adult↗
Successful radiofrequency catheter ablation from the supravalvular region of the aortic valve in a patient with outflow tract ventricular tachycardia.
Outflow tract ventricular tachycardia (OT-VT) was successfully ablated from the right coronary cusp of the aortic valve. The 12-lead ECG was totally different from the typical right ventricular OT-VT because the R/S ratio in precordial lead V1 was equal to 1 and tall R waves in precordial leads V2-6 were seen. Radiofrequency energy application from the right coronary cusp of the aortic valve successfully ablated this VT without complications. Radiofrequency catheter ablation from the right coronary cusp of the aortic valve can be done safely and effectively.
Aged↗
Lack of a relation between serum potassium concentration and exercise hyperpnea in patients with chronic heart disease.
Exertional dyspnea, a major symptom of patients with chronic heart failure, mainly stems from an abnormally high ventilatory response to exercise. However, there has been considerable controversy surrounding the mechanisms of respiratory control during exercise, especially regarding the role of serum potassium. We investigated the relation between serum potassium concentration [K+] and ventilation (VE) during exercise before and after oral supplements of potassium chloride in cardiac patients. Thirteen patients with chronic heart disease performed a 6-min constant-work-rate exercise (65.8+/-11.1 W) with respiratory gas measurements before initiating oral supplements of potassium chloride, 4 weeks after continued supplements, and 4 weeks after discontinuing supplements. Blood was sampled from a forearm vein at rest before exercise and at the end of exercise for measurement of [K+] and blood gases. The [K+] at rest was 3.66+/-0.30 mmol/L before oral supplements of potassium and significantly increased to 4.08+/-0.31 mmol/L (p<0.01) after supplements. In spite of the significant increases in the [K+], resting VE was not changed. While serum [K+] during exercise was significantly higher after potassium supplements than before, exercise VE was not influenced by the changes in [K+] throughout the study period. The findings of the present study strongly suggest that the chronic increase in the serum [K+] has no influence on the resting or exercise VE in patients with heart disease.
Adult↗
G1 cyclins are involved in the mechanism of cardiac myocyte hypertrophy induced by angiotensin II.
The importance of the cell cycle in proliferating cells is well known, but little is known about the role of cell cycle regulatory proteins in cardiac myocytes, which are fully differentiated cells. The present study determined, in vitro, the effect of angiotensin II (Ang II) treatment of neonatal rat cardiac myocytes on protein levels of cyclins and retinoblastoma gene product (pRb) phosphorylation. The role of G1 cyclin/cdk in Ang II-induced cardiac myocyte hypertrophy by overexpressing cdk inhibitor p21Cip1/Waf1 or p16INK4a was also examined using recombinant adenoviral vectors encoding these genes. Western blot analysis revealed that Ang II stimulated cyclin D1, D2, D3 and A protein levels in cardiac myocytes. Moreover, Ang II phosphorylated pRb on serine 780, which is known to occur in mitotic cells during cell cycle progression. Cultured cardiac myocytes treated with Ang II and infected with either control or recombinant adenovirus indicated that expression of p21 and p16 inhibited Ang II-induced cardiac myocyte hypertrophy, [3H]leucine incorporation into total cellular proteins, and skeletal alpha-actin (SK-A) and atrial natriuretic peptide (ANP) mRNA accumulation. Control virus had no effects on these parameters. These results suggest that G1 cyclins play an important role in cardiac myocyte hypertrophy stimulated by Ang II.
Angiotensin II↗
Role and relation of p70 S6 and extracellular signal-regulated kinases in the phenotypic changes of hypertrophy of cardiac myocytes.
Cardiac hypertrophy is characterized by increased cardiomyocyte protein synthesis, increased cell volume, and a shift in cardiac-specific gene expression to fetal isoforms. Using neonatal rat cardiomyocytes stimulated with fetal calf serum (FCS) as a model for cardiac hypertrophy, the present study investigated the role of 2 signal transduction pathways, extracellular signal-regulated kinase (ERK) and p70S6 kinase (p70S6K), in the attendant phenotype changes. FCS evoked both ERK and p70S6K activity, peaking at 20-40min, and simultaneously increased cardiac myocyte protein synthesis (evaluated by [3H]leucine incorporation and total cellular protein content), cell size (evaluated by morphometry and fluorescence-activated cell sorter analysis) and expression of a fetal isoform of the muscle specific gene skeletal alpha-actin (SKA). Rapamycin, a specific inhibitor of the mammalian target of rapamycin (mTOR), which is an upstream signaling of p70S6K, completely inhibited FCS-induced cell size increases and protein synthesis, but had no effect on SKA mRNA expression. PD98059, which inhibited ERK activity, attenuated cardiac-specific gene expression in a dose-dependent manner, but had no influence on protein synthesis or cell size. These results indicate divergent roles for the ERK and p70S6K pathways in the phenotypic changes associated with cardiac hypertrophy.
Actins↗
Prognostic significance of cardiopulmonary exercise testing for 10-year survival in patients with mild to moderate heart failure.
Although a number of studies have investigated the prognostic significance of exercise variables, they have focused only on short-term prognosis in relatively severe heart failure. This study was carried out to determine whether the indices obtained during cardiopulmonary exercise testing have prognostic significance during a 10-year follow-up in mild to moderate heart failure. Three hundred and sixty-four consecutive patients with cardiac disease performed 4 min of 20-W warm-up, followed by a symptom-limited incremental exercise test on a cycle ergometer. In addition to the measurements of peak oxygen uptake (VO2) and gas exchange (anaerobic) threshold, the time constant of VO2 kinetics during the onset of warm-up exercise was calculated using a single exponential equation. Data on mortality were available for follow-up in 260 patients. After 3,331+/-610 days of follow-up, 29 cardiovascular-related deaths occurred. The time constant of VO2 in the nonsurvivors was 76.7+/-43.3 s and was significantly prolonged compared with that of survivors (55.3+/-30.6 s, p=0.001). Peak VO2 and gas exchange threshold were both significantly lower in nonsurvivors than in survivors. Kaplan-Meier survival curves for 10 years of follow-up demonstrated a survival rate of 89.0% for patients with a normal VO2 time constant (< 80 s) and 71.7% for those with a longer time constant (> or = 80 s), showing a significant difference in survival (p=0.0028). Respiratory gas parameters obtained during exercise testing, particularly the time constant of VO2 kinetics, were found to be useful for predicting long-term prognosis in patients with chronic heart failure. These results suggest that cardiopulmonary exercise testing could be more applicable in ambulatory patients with minimal symptoms or minimal functional impairment.
Actuarial Analysis↗
Suppression of integrin alpha(v) expression by endothelin-1 in vascular smooth muscle cells.
Both integrins and endothelins (ETs) are known to play important roles in vascular remodeling via proliferation, apoptosis, and migration of vascular smooth muscle cells (VSMCs), whose dysfunctions have been implicated in the pathogenesis of end-organ damage associated with hypertension and arteriosclerosis. However, whether there is any interaction between endothelin-1 (ET-1) and integrins remains unknown. Therefore, the aim of the present study was to elucidate whether ET-1 regulates the expression of integrin alpha(v) in rat VSMCs. ET-1 dose- and time-dependently suppressed the integrin alpha(v) messenger RNA (mRNA) transcripts, as quantified by a real-time quantitative polymerase chain reaction (PCR) method, and decreased the transcriptional activity of integrin alpha(v) gene, as demonstrated by integrin alpha(v)-luciferase assay. The inhibitory effect of ET-1 on integrin alpha(v) gene expression was abrogated by an ETA receptor antagonist (BQ123) but not by an ET(B) receptor antagonist (BQ788). ET-1 also suppressed the cell surface expression of integrin alpha(v)beta5 and the adhesion to vitronectin, but not to fibronectin. These results demonstrate that the adhesion of vitronectin to rat VSMCs is inhibited by ET-1 via the ET(A) receptors by suppressing integrin alpha(v) gene transcription, suggesting that ET-1 is involved in regulation of vascular integrin alpha(v) gene expression.
Animals↗
Cytokine-activated p42/p44 MAP kinase is involved in inducible nitric oxide synthase gene expression independent from NF-kappaB activation in vascular smooth muscle cells.
Recent evidence suggests the possible involvement of inducible nitric oxide synthase (iNOS) in the development and maintenance of hypertension in certain animal models. Inflammatory cytokines activate nuclear factor (NF)-kappaB, which plays a major role in transactivation of the inducible nitric oxide synthase (iNOS) gene. However, it remains unknown whether cytokine-mediated iNOS expression in vascular smooth muscle cells (VSMCs) requires signaling pathway(s) other than NF-kappaB activation. The purpose of this study was to determine whether the p42/p44 MAP kinase pathway is involved in cytokine-induced NF-kappaB activation and/or iNOS expression in cultured rat VSMCs. Nitrite/nitrate (NOx) production stimulated by interleukin (IL)-1beta or tumor necrosis factor (TNF)-alpha in VSMCs was markedly suppressed by inhibiting MAP kinase by pretreatment with a p42/p44 MAP kinase kinase (MAPKK)-1 inhibitor (PD98059) or by transfecting the dominant-interfering form of the nonphosphorylated MAPKK-1 expressing construct (MAPKK S222A). Inhibition of p42/p44 MAP kinase also antagonized the upregulation of iNOS mRNA and protein, as demonstrated by the quantitative RT-PCR method and Western blot analysis, respectively. Furthermore, rat iNOS promoter activity using an iNOS-luciferase construct stimulated by cytokines was inhibited by MAPKK-1 inhibition. However, kappaB-dependent transcription analysis revealed that cytokine-stimulated NF-kappaB activity was unaffected by MAP kinase inhibition. Western blot analysis using anti-IkappaB-alpha and anti-phospho-IkappaB-alpha antibodies showed that PD98059 had no effect on transient phosphorylation or degradation of IkappaB-alpha by cytokines. An electrophoretic mobility shift assay using synthetic oligonucleotide corresponding to the downstream NF-kappaB site of rat iNOS promoter as a probe showed that MAP kinase inhibition did not block cytokine-stimulated activation of NF-kappaB. These data suggest that the MAP kinase pathway is in part involved in cytokine-induced iNOS expression independent from NF-kappaB activation in rat VSMCs.
Animals↗
Percutaneous transluminal coronary angioplasty improves oxygen uptake kinetics during the onset of exercise in patients with coronary artery disease.
STUDY OBJECTIVES: Although percutaneous transluminal coronary angioplasty (PTCA) is known to have beneficial effects on exercise capacity, its effects on the cardiovascular response during the onset of exercise have not been clarified. The present study was undertaken to determine the effects of PTCA on the kinetics of oxygen uptake (VO(2)) during constant-work-rate exercise in patients with coronary artery disease, as well as on their indexes of maximal work capacity. METHODS: Seventeen patients with coronary artery disease who received successful PTCAs performed a 50-W constant-work-rate exercise test for 6 min and a symptom-limited incremental exercise test both before and 4 months after the PTCA procedure. VO(2) was calculated from breath-by-breath analysis of respired gases. The time constant of VO(2) kinetics during the onset of 50-W exercise was determined by fitting a single exponential function to the VO(2) response. RESULTS: In 14 patients without coronary restenosis, the time constant of VO(2) kinetics was significantly shortened from (mean +/- SD) 57.4 +/- 12.6 before PTCA to 48.2 +/- 9.5 s after PTCA (p = 0. 0035), indicating improved kinetics of the VO(2) response. In these subjects, the peak VO(2) obtained during maximal exercise testing also increased from 23.1 +/- 3.5 to 26.5 +/- 3.2 mL/min/kg, respectively (p = 0.0005). However, there was no improvement in these indexes in the patients who had restenosis after undergoing PTCA (n = 3). CONCLUSION: Indexes of cardiopulmonary exercise testing, which reflect an efficiency of oxygen flow to the exercising muscle, can be used as an objective, noninvasive, and cost-effective guide for understanding which patients will not have coronary restenosis following PTCA.
Aged↗