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Biomedical subjects

J Soler-Soler

Publications and source records attributed to J Soler-Soler.

At least 37 records · Page 2Linked to original sources
PubMed1997

Lack of evidence of M-cells in porcine left ventricular myocardium.

OBJECTIVE: The aim of this study was to analyze whether cells with long action potential duration, fast Vmax, and spike-and-dome configuration (M-cells) are present in porcine left ventricular myocardium. METHODS: Transmembrane action potentials (n = 505) of the left ventricle were recorded with conventional glass microelectrodes in an epicardial-endocardial direction at 2000 ms basic cycle length in 14 pigs. In 3 pigs, potentials were obtained at 1000, 2000, and 5000 ms cycle length before and after superfusion with quinidine HCl 1 microgram/ml. In addition, transmembrane potentials (n = 52) were recorded in 4 dogs at 2000 ms cycle length to verify the ability of our protocol to detect M-cells. RESULTS: In pigs, action potential duration at 90% repolarization was shorter (ANOVA, P < 0.001) and Vmax slower (P < 0.001) in the epicardium than in the other transmural sites, but there were no regional differences in resting membrane potential or in action potential amplitude. Potentials with particularly long phase 3 or with spike-and-dome configuration were not observed. All myocardial sites displayed rate dependence of action potential duration (P = 0.02) which was transmurally homogeneous and persisted after quinidine exposure. The drug did not induce afterdepolarizations. In dogs, potentials with spike-and-dome configuration, long duration, and fast Vmax, like those described in M-cells, were detected in deep epicardial and midmyocardial areas. CONCLUSION: The porcine left ventricular myocardium shows transmural differences in action potential duration and Vmax, but, unlike dogs, it lacks M-cells.

Action Potentials↗
PubMed1997

Prevention of ischemic rigor contracture during coronary occlusion by inhibition of Na(+)-H+ exchange.

OBJECTIVE: To determine the effect of Na(+)-H+ exchange blockade on ischemic rigor contracture and reperfusion-induced hypercontracture. METHODS: Thirty-six pigs were submitted to 55 min of coronary occlusion and 5 h reperfusion. Myocardial segment length analysis with ultrasonic microcrystals was used to detect ischemic rigor (reduction in passive segment length change) and hypercontracture (reduction in end-diastolic length). RESULTS: Pretreatment with the new, highly selective Na(+)-H+ exchange inhibitor HOE642 before occlusion reduced ischemic rigor (P < 0.05), attenuated segment shrinkage (P < 0.05) during subsequent reperfusion, dramatically reduced infarct size (P < 0.0001) and attenuated arrhythmias (P < 0.01). Inhibition of Na(+)-H+ exchange only during reperfusion by means of direct intracoronary infusion of HOE642 into the area at risk prevented reperfusion arrhythmias but had no effect on final infarct size, while treatment with intravenous HOE642 immediately before reperfusion had no detectable effects. CONCLUSION: These results indicate that inhibition of Na(+)-H+ exchange during ischemia is necessary to limit myocardial necrosis secondary to transient coronary occlusion, and that this action could by mediated by a protective effect against ischemic contracture. Inhibition of Na(+)-H+ exchange only during reperfusion has a partial and transient beneficial effect, but only when the inhibitor reaches the area at risk before reflow.

Animals↗
PubMed1997

[Chronic total occlusion of the left main coronary artery].

Total chronic occlusion of the left main coronary artery is a rare angiographic finding in a catheterization laboratory. After reviewing the coronary angiographies performed in our laboratory between 1986 to 1995, we found a prevalence of 0.04%. These patients presented unspecific symptoms similar to other kinds of coronary artery disease. In all cases, the right coronary artery was dominant with extensive collateral circulation to the left coronary artery. Ventricular function was normal in 50% of the cases. Probably, in these unusual cases, the best therapeutic approach is surgical revascularization.

Aged↗
PubMed1997

Clinical outcome and long-term prognosis of late prosthetic valve endocarditis: a 20-year experience.

A prospective study of the clinical characteristics and evolutionary patterns of 59 cases of late prosthetic valve endocarditis (LPVE) that occurred between January 1975 and December 1994 was performed. Of these 59 cases of LPVE, 48 involved mechanical valves and 11 involved biological valves. Etiologies were as follows: streptococci, 41% of cases; staphylococci, 25%; enterococci, 13%; and miscellaneous, 21%. Echocardiography documented vegetations in 21 patients, paravalvular abscesses in 10, and prosthetic leaks in 34. Emboli occurred in 22 patients, and heart failure in 19 patients. Forty-two patients received medical treatment alone, and 17 received medical treatment and underwent valve replacement surgery. The in-hospital mortality rate was 25%; staphylococcal infection caused 67% of deaths, streptococcal infection caused 5%, and other etiologies caused 23% (P = .0004). After adjustment for age and type of prosthesis, multiple logistic regression revealed an odds ratio for death due to nonstreptococcal infections of 9.67. The overall survival rate was 59% at 5 years and 52% at 10 years. During follow-up, 17 patients needed new valves. At the end of follow-up, only 13 patients remained alive and had the same prosthesis that they had at the time of the diagnosis of LPVE.

Adolescent↗
PubMed1997

Severe mitral regurgitation complicating acute myocardial infarction. Clinical and angiographic differences between patients with and without papillary muscle rupture.

AIMS: To assess the differential clinical and angiographic characteristics of patients with severe mitral regurgitation related (n = 31) or unrelated (n = 16) to papillary muscle rupture complicating acute myocardial infarction. METHODS AND RESULTS: The clinical and angiographic features of patients with myocardial infarction and severe mitral regurgitation were evaluated. Patients with papillary muscle rupture were older (67 vs 60 years, P < 0.005) and had a lower rate of diabetes (7% vs 38%, P < 0.005) and of previous angina or infarction (24% vs 50%, P < 0.05). Frequency of inferior infarction was high and comparable in both groups (papillary muscle rupture, 72% vs non-papillary muscle rupture, 88%, ns) whereas in-hospital rate of angina/infarct extension prior to mitral regurgitation, also high, tended to be higher in patients without than in those with papillary muscle rupture (67% vs 39%, ns). Incidence of multivessel disease tended to be higher in patients without papillary muscle rupture (87% vs 56%, P < 0.06) and they had a lower ejection fraction (46 +/- 15 vs 61 +/- 14%, P < 0.03), whereas the culprit artery was mainly the right or the circumflex coronary artery in both groups (papillary muscle rupture, 100% vs non papillary muscle rupture, 93%, ns). Valve replacement was performed earlier in patients with papillary muscle rupture (1 (1; 14) vs 25 (5; 45) days, median, P < 0.002) but was associated with a similar mortality (papillary muscle rupture 11/24, 46% vs non-papillary muscle rupture, 7/15, 47%, ns). The main cause of death was cardiogenic shock in patients without papillary muscle rupture (5/7, 71%), and respiratory insufficiency--sepsis in those with papillary muscle rupture (7/11, 64%). CONCLUSIONS: Severe mitral regurgitation in myocardial infarction with or without papillary muscle rupture is mostly related to inferior infarction and often follows reinfarction, particularly in non-papillary muscle rupture cases. The main contributors to surgical mortality appear to be respiratory insufficiency in patients with papillary muscle rupture and cardiogenic shock, facilitated by a lower ejection fraction, a higher frequency of diabetes and more extensive coronary disease, in patients without papillary muscle rupture.

Aged↗
PubMed1997

Measuring functional status of chronic coronary patients. Reliability, validity and responsiveness to clinical change of the reduced version of the Duke Activity Status Index (DASI).

AIMS: Health-related quality of life assessment may be useful for understanding the variability in functioning of patients with a similar level of clinical impairment. We assessed the reliability, validity and responsiveness to clinical change of a reduced version of the Duke Activity Status Index (DASI) in chronic coronary patients. METHODS AND RESULTS: The reduced version of the DASI, a measure of self-reported functional capacity, was administered twice to two groups of patients: 46 stable coronary heart disease outpatients were tested and re-tested 2 weeks after their initial visit; and 44 patients undergoing elective angioplasty for angina pectoris were evaluated the day before and one month after the procedure. The Canadian Cardiovascular Society (CCS) functional grade was assessed in all patients, and a treadmill exercise test was performed sequentially (before and after the procedure) in angioplasty patients. Cronbach's alpha reliability coefficients for reduced DASI scores were high (between 0.81 and 0.89). Correlations of the reduced DASI scores with CCS grade and exercise test duration were moderately high (r = -0.51 and r = 0.45, respectively). Improvement after angioplasty as assessed by the reduced DASI scores was important (effect size = 0.75, P < 0.001). CONCLUSION: The reduced DASI is reliable, valid and responsive to clinical changes. Health-related quality of life measures may be useful in monitoring coronary patients.

Activities of Daily Living↗
PubMed1997

Local repolarization abnormalities induced by transcatheter radiofrequency ablation in pigs.

Radiofrequency (RF) ablation alters action potential repolarization of myocardial cells and, theoretically, this should induce ST-T segment changes in the ECG. Since these ECG abnormalities have been rarely reported in patients submitted to RF ablation we assess the ability of the procedure to cause ST-T segment changes in local electrograms. Epicardial ECG mapping was performed in 17 anesthetized open chest pigs submitted to endocardial (n = 9) or to epicardial (n = 8) unipolar radiofrequency ablation (500 kHz, 20 W for 5-10 s). To characterize the cellular electrophysiological alterations induced by RF ablation transmembrane action potentials were recorded at various distances from the ablation lesion; these were compared with seven control pigs. Endocardial RF ablation induced a transient (< 5 min) change of 6.1 +/- 2.4 mV in T wave amplitude (baseline: 12.8 +/- 5.6 mV, P < 0.001) in 141 out of 269 epicardial electrodes. T wave changes were associated with shortening in local activation time (20.1 +/- 2.3 ms at baseline vs 18.5 +/- 2.5 ms at 60 s after ablation, P = 0.03). RF current caused persistent St segment elevation at the center of the ablation lesion with no transmural expansion. Intracellular potentials along a 2-6 mm wide myocardial band bordering the RF lesion lower amplitude (101 +/- 7.0 mV vs 71 +/- 23 mV, P < 0.01) and shorter duration (254 +/- 44 ms vs 156 +/- 29 ms, P < 0.01) than control hearts. The center of the ablation lesion was electrically unexcitable. We concluded that RF ablation alters cellular electrophysiology in small areas surrounding the ablation lesion and this causes short-lasting transmural changes in T 3 wave amplitude and nontransmural ST segment elevation.

Action Potentials↗
PubMed1997

Myocardial necrosis by electrocution: evaluation of noninvasive methods.

We present the case of a young man who suffered severe anteroapical myocardial necrosis caused by electrocution. In addition to the enzymatic and electrocardiographic changes suggesting necrosis, a clear positive segmental image on 99mTc-pyrophosphate scintigraphy and a defect on a 201Tl SPECT scan at rest were also found. Although these tests were indicative of extensive anteroapical transmural myocardial necrosis, the echocardiographic study only revealed mild anteroapical hypokinesia.

Adult↗
PubMed1996

Neurally mediated negative inotropic effect impairs myocardial function during cholinergic coronary vasoconstriction in pigs.

BACKGROUND: Myocardial dysfunction elicited during cholinergic coronary vasospasm is generally ascribed to myocardial ischemia. However, when pericoronary nerves extend to the ventricles, efferent vagal discharges that elicit coronary vasoconstriction may, at the same time, depress myocardial contractility by releasing acetylcholine into the myocardium. We analyzed whether a neurally mediated effect contributes to impairment of ventricular function during cholinergic coronary vasoconstriction. METHODS AND RESULTS: Left ventricular (LV) function, ECG mapping, and coronary angiography were analyzed during pericoronary application of methacholine (MCh) to the left anteriors. descending coronary artery in 53 chloralose-anesthetized openchest pigs. MCh induced local coronary vasoconstriction and depressed coronary blood flow (13.3 +/- 3.7 to 6.0 +/- 4.6 mL/min [54%]; ANOVA, P < .001), systolic LV pressure (105 +/- 10 to 91 +/- 10 mm Hg [13%], P < .001), peak LV (+)dP/dt (2890 +/- 524 to 2270 +/- 447 mm Hg/s [21%], P < .001), peak LV (-)dP/dt (1446 +/- 484 to 1048 +/- 276 mm Hg/s [27%], P < .001), and regional systolic segment shortening (0.32 +/- 0.09% to 0.18 +/- 0.14% [43%], P = .02) and caused local ST-segment elevation (0.9 +/- 0.8 to 8.4 +/- 3.9 mV, P < .001). These changes were not preceded by heart rate variations, were reproducible, and were inhibited by atropine. MCh during perfusion of nitroglycerin (2 micrograms.kg-1.min-1 IV) continued to depress LV pressure (9%, P = .002), LV (+)dP/dt (16%, P < .01), LV (-)dP/dt (20%, P < .01), and segment shortening (18%, P = .03) even though coronary blood flow drop was markedly attenuated (7% versus 54%; ANOVA, P < .01). Disruption of pericoronary nerves with phenol attenuated MCh-induced LV pressure fall (P < .05). Histological data show that cholinergic and adrenergic pericoronary nerves extend into the ventricular myocardium. CONCLUSIONS: A neurally mediated effect, in addition to ischemia, impairs LV function during cholinergic coronary constriction in a model with pericoronary nerves extending into the ventricles.

Animals↗
PubMed1996

Comprehensive noninvasive assessment of cardiac involvement in limited systemic sclerosis.

OBJECTIVE: To assess cardiovascular abnormalities in patients with limited systemic sclerosis (SSc), using noninvasive cardiac techniques. METHODS: Sixty-three patients with limited SSc were prospectively evaluated with Doppler echocardiography and thallium-201 perfusion scintigraphy after a cold-stress test and radionuclide ventriculography. RESULTS: In the patients with limited SSc, there was a significantly high prevalence of abnormal left- and right-diastolic function parameters (P = 0.001 and P = 0.0002, respectively), thickening of papillary muscles (46%; P = 0.003), and mild mitral regurgitation (49%; P < 0.0001), compared with controls. Systolic pulmonary arterial hypertension was detected in 9 patients (14%), and pericardial effusion in 11 patients (18%). In 64% of patients with limited SSc, an ischemic response was detected on the thallium cold-stress scan; similarly, an ischemic response was detected in 57% of patients with primary Raynaud's phenomenon (P < 0.0001 versus controls). CONCLUSION: Although the frequency of cardiovascular symptoms was low in patients with limited SSc, a significant rate of cardiovascular abnormalities was found by noninvasive cardiac techniques.

Adult↗
PubMed1996

Intimal injury in a transiently occluded coronary artery increases myocardial necrosis. Effect of aspirin.

This study tested the hypothesis that intimal injury in a transiently occluded coronary artery limits myocardial salvage. The effect of intimal injury on reactive hyperaemia was investigated in 17 pigs submitted to a 30-min occlusion of the left anterior descending coronary artery (LAD), not resulting in myocardial infarction. Catheter-induced intimal damage increased local platelet deposition (99mTc) and reduced hyperaemia, but did not modify myocardial platelet or polymorphonuclear leucocyte content (myeloperoxidase activity) after 6 h reperfusion. To investigate the influence of intimal injury on the extent of myocardial necrosis secondary to a more prolonged coronary occlusion, and the role of platelets on this influence, 52 pigs were submitted to a double randomization (2x2 factorial design) to 250 mg i.v. aspirin vs. placebo and to coronary intimal injury vs. no coronary damage before a 48-min occlusion of the LAD and 6 h of reperfusion. After excluding 12 animals with reocclusion, coronary intimal injury was associated with larger infarcts (triphenyltetrazolium reaction) in animals receiving placebo (36.2+/-7.0% of the area at risk in animals with intimal injury vs. 10.8+/-3.9% in animals without coronary injury, P=0.006) but not in those receiving aspirin (20.3+/-6.5 vs. 21.7+/-6.5% of the area at risk in animals with and without intimal injury respectively). These results suggest that coronary intimal injury in the reperfused artery may have adverse effects on myocardial salvage by mechanisms other than reocclusion or embolization of platelet aggregates.

Animals↗
PubMed1996

Coronary denervation attenuates coronary constriction induced by muscarinic receptor stimulation in pigs.

OBJECTIVES: We tested the hypothesis that coronary denervation attenuates the reactivity of the coronary vessel to cholinergic stimulation. METHODS: Heart rate, left ventricular (LV) pressure, LV dP/dt, coronary blood flow at the left anterior descending (LAD) coronary artery, and epicardial ECG mapping were measured before and after topical application of 1% methacholine to the LAD in 10 pigs anesthetized with alpha-chloralose (100 mg/kg, i.v.); these were compared with 10 other pigs submitted 2 weeks previously to a denervation of the LAD with phenol. Coronary denervation was confirmed in all cases by adrenergic histofluorescence and by acetyl-cholinesterase staining. Isolated LAD rings from 10 additional pigs (5 controls and 5 treated with phenol) were stimulated with endothelin-1 to verify whether phenol affected coronary reactivity to noncholinergic stimulation. RESULTS: Methacholine induced a fall in coronary blood flow (10.3 +/- 5.3 ml/min vs 4.8 +/- 6.2 ml/min, ANOVA: P < 0.001), a drop in systolic LV pressure (113 +/- 19 mmHg vs 93 +/- 19 mmHg, P < 0.001) and LV dP/dt (1608 +/- 363 mmHg/s vs 1203 +/- 302 mmHg/s, P = 0.02) and elevation of the ST segment (1.4 +/- 0.9 vs 11.1 +/- 4.7 mV, P < 0.001) in controls. These changes were not preceded by heart rate variations and were inhibited by atropine. As compared to controls, phenol-treated pigs showed a smaller decline in coronary blood flow (13.1 +/- 4.5 ml/min to 10.4 +/- 5.4 ml/min, P < 0.001), a lower drop in LV pressure (107 +/- 20 mmHg to 100 +/- 19.7 mmHg, P < 0.001) and lesser ST segment elevation (2.2 +/- 1.7 mV to 5.6 +/- 4.2 mV, P < 0.001). Isolated LAD rings contracted after exposure to endothelin-1 in both controls and phenol-treated pigs (3.5 +/- 0.7 g vs 2.4 +/- 1.0 g, P = 0.06). CONCLUSIONS: Coronary denervation attenuates coronary constriction induced selectively by direct muscarinic receptor stimulation in the in situ pig heart.

Animals↗
PubMed1996

Diagnosis of ascending aortic dissection by transesophageal echocardiography: utility of M-mode in recognizing artifacts.

OBJECTIVES: This study sought to assess the reliability of biplanar transesophageal echocardiography in the diagnosis of ascending aortic dissection and to test the utility of M-mode information in the differential diagnosis of ascending aortic ultrasound artifacts and intimal flap images. BACKGROUND: Transesophageal echocardiography is a useful technique in the diagnosis of aortic dissection. However, ultrasound artifacts in the ascending aorta are an important limitation. METHODS: Transesophageal echocardiography was performed in 132 consecutive patients with clinically suspected aortic dissection. Two-dimensional and M-mode echocardiography and color Doppler were used to diagnose intimal flap and artifact images. Diagnoses were validated either anatomically or with reference techniques. RESULTS: The sensitivity and specificity of transesophageal echocardiography in the diagnosis of ascending aortic dissection were 96.8% and 100%, respectively. Ninety-three artifacts were observed in 56 (55%) of 101 patients without ascending aortic dissection. Two-dimensional echocardiography easily identified 74 artifacts (80%). Color Doppler showed no ascending flow abnormalities in 71% of artifact images. M-mode echocardiography showed three location and mobility artifact patterns related to the posterior wall of the aorta or the right pulmonary artery. In contrast, intimal flap movement showed no relation to the aortic wall movement in 25 cases (83%). Blind analysis of transesophageal echocardiographic study tapes underlined the utility of M-mode in the differential diagnosis. Ranges of sensitivity, specificity and positive predictive value (established by including doubtful results as either positive or negative) improved from 87.1-93.5% to 93.5-96.8%, from 85.1-94.1% to 99-100% and from 65.9-81.8% to 96.8-100%, respectively, with the inclusion of M-mode data. CONCLUSIONS: Biplanar transesophageal echocardiography permits reliable diagnosis of ascending aortic dissection. Ultrasound artifacts are common, but assessment of the location and mobility of intraluminal images by M-mode echocardiography definitely improves diagnostic accuracy.

Adolescent↗
PubMed1996

Intravenous amiodarone in treatment of recent-onset atrial fibrillation: results of a randomized, controlled study.

OBJECTIVES: This study was designed to determine the efficacy of intravenous amiodarone in the management of recent-onset atrial fibrillation. BACKGROUND: The optimal approach for acute atrial fibrillation has not been established. Amiodarone is a unique antiarrhythmic agent with activity in both supraventricular and ventricular tachyarrhythmias, but its value for the restoration of sinus rhythm in patients with recent-onset atrial fibrillation has not been demonstrated. METHODS: Sample size was calculated to detect a 25% increase in reversion rate with amiodarone with a statistical power of 80%. One hundred consecutive patients with recent-onset (<1 week) atrial fibrillation and not taking antiarrhythmic agents were randomized to receive either intravenous amiodarone, 5 mg/kg body weight in 30 min followed by 1,200 mg over 24 h, or an identical amount of saline. Both groups received intravenous digoxin, 0.5 mg initially, followed by 0.25 mg at 2 h and 0.25 mg every 6 h thereafter, to complete 24 h while the ventricular rate was >100 beats/min. Amiodarone and digoxin blood levels were determined. Both groups were homogeneous regarding underlying heart disease, time from onset to treatment, initial ventricular rate and left atrial size. RESULTS: By the end of the 24-h treatment period, 34 patients (68%, 95% confidence interval [CI] 53% to 80%) in the amiodarone group and 30 (60%, 95% CI 45% to 74%) in the control group had returned to sinus rhythm (p = 0.532). Mean times (+/-SD) of conversion were 328 +/- 335 and 332 +/- 359 min, respectively (p =0.957). Among patients who did not convert to sinus rhythm, treatment with amiodarone was associated with a slower ventricular rate (82 +/- 15 beats/min in the amiodarone group vs. 91 +/- 23 beats/min in the control group, p = 0.022). After restoration of sinus rhythm, atrial fibrillation recurred during a 15-day follow-up period in 4 (12%) of 34 patients (95% CI 3% to 27%) in the amiodarone group and in 3 (10%) of 30 (95% CI 2% to 26%) in the control group (p = 0.861). CONCLUSIONS: Intravenous amiodarone, at the doses used in this study, produces a modest but not significant benefit in converting acute atrial fibrillation to sinus rhythm.

Adult↗
PubMed1996

Reliability of electromechanical dissociation in the diagnosis of left ventricular free wall rupture in acute myocardial infarction.

The reliability of electromechanical dissociation (EMD) in diagnosing acute left ventricular free wall rupture (LVFWR) was assessed in 479 consecutive patients with acute myocardial infarction (AMI). EMD was the mechanism of death in 193 patients, 140 without heart failure (group A, 74%), and 53 with heart failure (group B, 26%). Autopsies performed on 121 patients with EMD showed LVFWR in 81 (95%) of 85 from group A and in 7 (17%) of 36 from group B. Of the 106 patients without EMD (group C) autopsied, 5 (4.7%) had LVFWR. Excluding the eight patients with associated septal rupture, LVFWR occurred in 79 (95.2%) of 83 patients from group A, 4 (12.1%) of 33 from group B, and 2 (1.9%) of 103 from group C. Predictive accuracy of EMD for LVFWR in group A was 95% but only 17% in group B. Moreover, in 13 consecutive cases with a first AMI without heart failure and EMD, emergency surgery demonstrated LVFWR in all. Thus EMD has a highly predictive accuracy in diagnosing LVFWR in patients with a first AMI without overt heart failure.

Aged↗
PubMed1996

Pre-treatment with trimetazidine increases sarcolemmal mechanical resistance in reoxygenated myocytes.

OBJECTIVE: Cytoskeletal and sarcolemmal fragility secondary to anoxia may contribute to sarcolemmal rupture and cell death during reoxygenation of cardiomyocytes. This study investigated the influence of trimetazidine (TMZ), a drug with effects on lipid metabolism and cell membranes, on reoxygenation-induced sarcolemmal rupture. METHODS: Isolated adult rat myocytes were submitted to 60 min of metabolic inhibition and 5 min of hypo-osmotic reoxygenation to simulate reperfusion edema in situ. Cells were allocated to 3 groups of treatment: in one group, TMZ 100 mumol/l was added to both the metabolic inhibition and reoxygenation buffers (group TMZ); another group was submitted to the same treatment but cells had previously been incubated with TMZ 100 mumol/l for 3 h (group TMZ-Pre); a control group underwent metabolic inhibition and hypo-osmotic reoxygenation without any treatment. Cell morphology was monitored throughout the experiment and sarcolemmal integrity was assessed by quantification of LDH activity and trypan blue exclusion test. RESULTS: After 60 min of metabolic inhibition most cells (83.1 +/- 2%) presented rigor contracture without between-group differences. Reoxygenation resulted in hypercontracture of 84.2 +/- 2.3, 91.2 +/- 1.4 and 84.1 +/- 2.1% of cells in TMZ, TMZ-Pre and control groups, P = NS. The trypan blue exclusion test revealed a higher proportion of cells with sarcolemmal integrity in TMZ and TMZ-Pre groups than in controls (12.7 +/- 2.0, 10.0 +/- 1.5 and 6.3 +/- 0.8%, respectively, P = 0.002). No between-group differences in LDH activity in the extracellular medium were observed at the onset or at the end of metabolic inhibition. However, LDH release was significantly lower (P = 0.002) in the TMZ-Pre group (1.6 +/- 0.1 IU/1000 cells) than in the TMZ and control groups (1.9 +/- 0.2 and 2.2 +/- 0.1 IU/1000 cells). CONCLUSION: Preincubation of cardiomyocytes with TMZ does not prevent rigor contracture induced by metabolic inhibition or hypercontracture during subsequent reoxygenation, but does improve sarcolemmal resistance to reoxygenation-induced mechanical stress. This could help to explain the beneficial effect of TMZ on infarct size.

Animals↗
PubMed1996

Predisposing factors and prognostic value of sustained monomorphic ventricular tachycardia in the early phase of acute myocardial infarction.

OBJECTIVES: The purpose of the study was to analyze the factors that favor the occurrence of sustained monomorphic ventricular tachycardia in the early phase (< 48 h) of acute myocardial infarction and to establish its prognostic implications. BACKGROUND: Sustained monomorphic ventricular tachycardia early in the course of an acute myocardial infarction is an uncommon arrhythmia, and its significance has not been specifically studied. METHODS: The clinical characteristics and prognosis of sustained monomorphic ventricular tachycardia were studied in 21 (1.9%) of 1,120 consecutive patients admitted to the coronary care unit with a diagnosis of myocardial infarction. RESULTS: Patients with sustained monomorphic ventricular tachycardia had a larger infarct on the basis of peak creatine kinase, MB fraction (CK-MB) isoenzyme activity (435 +/- 253 IU/liter vs. 168 +/- 145 IU/liter, p < 0.001) and higher mortality rate (43% vs. 11%, p < 0.001). By logistic regression analysis, independent predictors of sustained monomorphic ventricular tachycardia were CK-MB (odds ratio [OR] 11.8), Killip class (OR 4.0) and bifascicular bundle branch block (OR 3.1). Moreover, sustained monomorphic ventricular tachycardia was itself an independent predictor of mortality (OR 5.0). Compared with patients with ventricular fibrillation, those with sustained monomorphic ventricular tachycardia had a worse Killip class (Killip class > I: 63% vs. 30%, p < 0.05), higher CK-MB activity (430 +/- 260 IU/liter vs. 242 +/- 176 IU/liter, p < 0.01) and higher arrhythmia recurrence rate (31% vs. 4%, p < 0.01). During the follow-up period, 5 (42%) of 12 survivors in the sustained monomorphic ventricular tachycardia group died of cardiac-related causes. Recurrence of ventricular tachycardia was seen in two patients (17%). CONCLUSIONS: Sustained monomorphic ventricular tachycardia during the first 48 h of myocardial infarction is a sign of extensive myocardial damage and an independent predictor of in-hospital mortality.

Adult↗