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Biomedical subjects

J Cinca

Publications and source records attributed to J Cinca.

At least 19 recordsLinked to original sources
PubMed2005

Identification of cardiomyogenic lineage markers in untreated human bone marrow-derived mesenchymal stem cells.

BACKGROUND: Recent reports refute the classic paradigm by which human heart is unable to repair itself following disease or injury. Cardiac and noncardiac stem cells with cardiac regeneration potential have been documented. We studied whether untreated mesenchymal stem cells express markers of cardiomyogenic lineage in vitro. METHODS: Mesenchymal stem cells were obtained from human iliac crest marrow aspirates. Cells were isolated and characterized using flow cytometry by surface expression of CD105, CD166, CD29, CD44, CD14, and CD34. To evaluate their cardiomyogenic potential, presence of cardiac proteins (cardiac troponin I, sarcomeric alpha-actinin, beta myosin heavy chain (beta-MyHC), connexin-43, and SERCA-2), and transcription factors (GATA-4) were assessed. RESULTS: Mesenchymal stem cells expressed CD105 (4.25 +/- 0.35), CD166 (27.83 +/- 1.89), and CD29 (9.4 +/- 0.57) and were negative for CD34, CD14, and CD45. In absence of additional stimuli in the culture media, these cells expressed connexin-43, alpha-actinin, and GATA-4, and were negative for SERCA-2, cardiac troponin I, and beta-MyHC. CONCLUSIONS: Human adult mesenchymal stem cells spontaneously exhibit markers of cardiac phenotype in vitro. In the appropiate myocardial environment, these cells may transdifferentiate into mature cardiomyocytes.

Adult↗
PubMed2000

Cardiovascular reflex responses induced by epicardial chemoreceptor stimulation.

The cardiac mechano- and chemoreceptors are broadly distributed in the myocardium and coronary vessels. A portion of these receptors extends over the epicardium and pericardium and therefore can be excited by mechanical or chemical stimuli directly applied to the surface of the heart. Excitation of epicardial receptors by topical application of chemical compounds elicits a variety of reflex cardiovascular responses, without the vascular or systemic effects of the drug administered systemically. A considerable number of studies has used the epicardial sensory field as a tool to delineate the functional characteristics of the cardiac afferent neurones in normal as well as in pathological conditions. In this review we analyze the cardiovascular reflex responses induced by epicardial application of a variety of substances like bradykinin, nicotine, muscarine, isoprenaline, adenosine, potassium chloride, capsaicin, prostaglandins or substance P in physiological models and also in models with acute myocardial ischemia or heart failure. The data highlight the contribution of the epicardial sensory neurites to the overall control of the cardiovascular system and, on the other hand, strengthen the need for further investigations directed to better elucidate the reflex cardiovascular responses that may develop in patients with pericardial abnormalities.

Animals↗
PubMed2000

Neurally mediated depressor hemodynamic response induced by intracoronary catheter balloon inflation in pigs.

OBJECTIVES: To assess whether intracoronary catheter balloon inflation triggers a neurally mediated hemodynamic response that interacts with the ischemia-induced myocardial dysfunction. METHODS: Forty-eight chloralose anesthetized pigs underwent a 60 s intraluminal catheter balloon inflation of the proximal left anterior descending (LAD) coronary artery before and after one of these treatments: disruption of LAD pericoronary nerves with phenol (n=6), bilateral stellectomy (n=8), bilateral cervical vagotomy (n=6), atropine (n=5), and ganglionic blockade with hexamethonium (n=10). In 13 other pigs, we assessed the reproducibility of two balloon inflations spaced 15 min (n=6) or 60 min (n=7). The ECG, left ventricular (LV) pressure, and LV dP/dt were recorded during each intervention. Right ventricular (RV) pressure, RV dP/dt, and aortic blood flow were also measured in a subset of pigs. RESULTS: Balloon inflation induced an early (10 s) and reproducible (ANOVA, P<0.001) drop in systolic pressure and peak dP/dt; a decrease in aortic blood flow; a rise in end-diastolic pressure; and elevation of the ST segment. Pericoronary denervation, stellectomy and ganglionic blockade attenuated (P<0.001) the drop in LV parameters during coronary inflation, but atropine and vagotomy did not. CONCLUSIONS: A depressor hemodynamic response subserved by pericoronary nerves worsens the LV dysfunction induced by brief coronary catheter balloon inflation in anesthetized pigs. Cholinergic fibers do not appear to play a major role.

Analysis of Variance↗
PubMed2000

Percutaneous electrocatheter technique for on-line detection of healed transmural myocardial infarction.

Healed myocardial infarction has been recognized by its particular tissue electrical impedance spectrum measured with intramural needle electrodes in animal models. The aim of this study was to develop a percutaneous approach for in vivo recognition of areas of healed myocardial infarction by measuring myocardial electrical impedance with an intracavitary contact electrocatheter. Electrical impedance (resistance and phase angle) of normal myocardium and of a 2-month-old anterior transmural infarction were measured in nine chloralose anesthetized pigs by applying alternating currents from 1 kHz to 1 MHZ between a bipolar intracavitary catheter and a reference electrode placed on the epicardium (group I, n = 4) or on the precordium (group II, n = 5). Resistance of the infarcted myocardium was lower than that of healthy tissue at all current frequencies (ANOVA, P < 0.001) (i.e., at 1 kHz: 15 +/- 4 omega vs 50 +/- 19 omega in group I, and 64 +/- 13 omega vs 76 +/- 13 omega in group II). Phase angle at 316 kHz best differentiated transmural infarction from normal tissue (group I: -2.5 +/- 1.9 degrees vs -14.8 +/- 4.6 degrees, P < 0.001; group II: +0.7 +/- 1.0 degrees vs -2.7 +/- 1.4 degrees, P < 0.001). This study shows that analysis of myocardial impedance spectrum using a percutaneous intracavitary contact catheter approach permits on-line recognition of areas of healed transmural myocardial infarction. This technique may be useful to optimize clinical application of energy sources (i.e., radiofrequency ablation, laser myocardial revascularization).

Analysis of Variance↗
PubMed1999

In vivo and in situ ischemic tissue characterization using electrical impedance spectroscopy.

The investigation of processes of ischemia in different organ tissues is very important for the development of methods of protection and preservation during surgical procedures. Electrical impedance spectroscopy was used to distinguish between different tissues and their degree of ischemia. We describe mathematical methods used to adjust experimental data to Cole-Cole models for one-circle and two-circle impedance loci and a study of the main parameters for representing the behavior of ischemia in time. In vivo and in situ postmortem measurements of different tissues from pigs are shown in the 100 Hz to 1 MHz range. The Cole parameters that best characterize the ischemia are R0 and fc.

Animals↗
PubMed1999

[Sudden death (II). Myocardial ischemia and ventricular arrhythmias in experimental models: triggering mechanisms].

Metabolic and electrolytic alterations generated in the acute ischemic myocardium, such as an increase in extracellular potassium or acidosis, are responsible for the occurrence of ventricular arrhythmias. In the first 5-10 minutes following coronary occlusion, reentry seems to have an important role, although not in the next 15 minutes. If the patient survives, a subacute arrhythmia period appears, 6 to 72 hours after the onset of ischemia, probably due to abnormal automaticity in the surviving Purkinje fibers. Finally, reentry in the epicardial border zone is the most likely mechanism for chronic arrhythmias. In this review we focus on the studies dealing with the mechanisms of ischemia-induced arrhythmias, with special reference to those conducted in experimental models.

Arrhythmias, Cardiac↗
PubMed1998

Differential uptake of myocardial perfusion radiotracers in normal, infarcted, and acutely ischemic peri-infarction myocardium.

OBJECTIVES: We measured the uptake of technetium-99m tetrofosmin (99m Tc) and thallium-201 (201 TI) in areas of healed transmural myocardial infarction and in the regions of acute peri-infarction ischemia. METHODS: Anesthetised pigs with a 1-month old transmural infarction elicited by permanent ligature of the left anterior descending (LAD) coronary artery below the first branch underwent one hour of proximal LAD occlusion followed by injection of 99m Tc-tetrofosmin and 201TI either in the left atrium (GI, n= 19) or in the jugular vein (GII, n = 6). Twelve other pigs (GIII) with similar acute peri-infarction ischemia received 99m Tc-tetrofosmin and 201Tl into the left ventricle during cardiocirculatory arrest to rule out the effect of coronary collaterals. Radiotracer counting was determined in samples from normal, acute ischemic and necrotic regions. RESULTS: Uptake of 99m Tc-tetrofosmin and 201 Tl was greater in the infarct scar (median % of normal tissue: 20 for 99m Tc and 8.6 for 201 Tl in GI; 22 and 15 in GII) than in acute ischemic myocardium (3.2 and 2.5 in GI; 6.4 and 3.3 in GII). Radiotracer injection in arrested hearts (GIII) depicted a similar pattern (median % of injected dose: 6.2 for 99m Tc and 10 for 201Tl in the scar; 2.3 and 4.0 in acute ischemia; 2.9 and 3.5 in normal tissue). The infarcted region showed connective tissue and lack of viable myocardium. CONCLUSION: A 1-month old infarct scar with no viable myocardial tissue can take up significant fractions of 99mTc-tetrofosmin and 201Tl even in the absence of coronary collateral perfusion. Data suggest that the infarct scar can extract these radiotracers from the intraventricular blood.

Animals↗
PubMed1998

Passive transmission of ischemic ST segment changes in low electrical resistance myocardial infarct scar in the pig.

OBJECTIVES: To analyze the passive electrical properties of a healed infarction and assess their role on transmission of contiguous ischemic ST segment potential changes. METHODS: We measured tissue resistivity (omega cm) at 1 kHz and the epicardial ST segment during 1 h of proximal reocclusion of the left anterior descending (LAD) coronary artery in 12 anesthetized pigs with one-month-old transmural infarction elicited by LAD ligature below the first branch. The impedance spectrum (1 to 1000 kHz) of normal and infarcted myocardium was measured in seven other pigs with similar infarctions. Electrical transmission of current pulses (30 microA) in infarcted tissue and in test solutions was also investigated. RESULTS: The infarct scar has a lower than normal resistivity (110 +/- 30 omega cm vs. 235 +/- 60 omega cm, p < 0.0001) and, unlike the normal myocardium, resistivity and phase angle of the scar did not change at increasing current frequencies, reflecting no capacitative response. LAD reocclusion induced a resistivity rise (510 +/- 135 omega cm, p < 0.01) and a ST segment elevation (0.6 +/- 0.7 to 9.5 +/- 5.1 mV, p = 0.002) in the ischemic peri-infarction zone, whereas the infarcted area showed ST segment elevation (0.5 +/- 0.5 to 3.8 +/- 2.6 mV, p = 0.03) with no resistivity changes. Potential decay of both ST segment and current pulses in the scar and in 0.9% NaCl solution was less than 1 mV/mm. Transmural deposition of connective tissue was seen in the center of the infarction. CONCLUSIONS: A one-month-old transmural infarction is a low resistance, noncapacitative medium that allows a good transmission of current pulses and of ST segment potential changes generated by contiguous peri-infarction ischemia.

Animals↗
PubMed1998

[National Registry of Automatic Implantable Defibrillators in 1996].

The results of the Spanish Registry of Automatic Defibrillators implanted between February 1996 and January 1997 are reported. A questionnaire per patient was completed by every implanting physician, in every center. The questionnaire was designed by the Section of Electrophysiology and Arrhythmias of the Spanish Society of Cardiology. The data from 306 automatic defibrillators implanted were reported. The percentage of defibrillators per inhabitant in Spain is close to 1 per 100,000. Eighty-five percent were first implants, while a 13% were replacements. Most of the electrodes used were endocardial. Chronic ischemic heart disease was found in 54% of the patients. Forty-six percent of the patients had syncopal ventricular tachycardia, 31% ventricular fibrillation and 23% sustained monomorphic ventricular tachycardia. The generator pocket was pectoral in 87% of the patients and abdominal in 13%. The implant of the defibrillator was associated with other cardiac surgery in only 3% of the patients.

Aged↗
PubMed1997

Changes in myocardial electrical impedance induced by coronary artery occlusion in pigs with and without preconditioning: correlation with local ST-segment potential and ventricular arrhythmias.

BACKGROUND: Myocardial ischemia increases tissue electrical resistivity leading to cell-to-cell uncoupling, and this effect is delayed by ischemic preconditioning in isolated myocardium. Alterations in myocardial resistivity elicited by ischemia in vivo may influence arrhythmogenesis and local ST-segment changes, but this is not well known. METHODS AND RESULTS: Myocardial impedance (resistivity [omega x cm] and phase angle [degrees]), epicardial ST segment, and ventricular arrhythmias were analyzed during 4 hours of coronary artery occlusion in 11 anesthetized open-chest pigs; these were compared with 13 other pigs submitted to a similar coronary occlusion preceded by ischemic preconditioning. Myocardial resistivity rose slowly during the first 34+/-7 minutes of occlusion (237+/-41 to 359+/-59 omega x cm), increased rapidly to 488+/-100 omega x cm at 60 minutes, and reached a plateau value (718+/-266 omega x cm, ANOVA; P<.01) at 150+/-69 minutes. By contrast, phase-angle changes began after 17 minutes of ischemia (-3.0+/-1.6 degrees to -4.2+/-1.2 degrees at 29+/-8 minutes) and evolved faster thereafter (-12.5+/-5.3 degrees at 144+/-56 minutes). Marked changes in myocardial impedance were observed during the reversion of ST-segment elevation that occurred 1 to 4 hours after occlusion, but impedance changes were less apparent during the early ST-segment recovery seen at 15 to 35 minutes of ischemia. The second arrhythmia peak (30+/-5 minutes) coincided with the fast change in tissue impedance, and both were delayed (P<.05) by ischemic preconditioning. CONCLUSIONS: A rapid impairment of myocardial impedance occurs after 30 minutes of coronary occlusion, and its onset is better defined by shift in phase angle than by rise in tissue resistivity. Phase 1b arrhythmias are associated with marked impedance changes, and both are delayed by preconditioning. Reversion of ST-segment elevation is partially associated with impairment of myocardial impedance, but other factors play a role as well.

Animals↗
PubMed1997

Acute ischemic ventricular arrhythmias in pigs with healed myocardial infarction: comparative effects of ischemia at a distance and ischemia at the infarct zone.

BACKGROUND: The myocardium bordering a healed infarction undergoes electrophysiological and autonomic neural derangements that may interact with a new ischemic episode to promote arrhythmias. Therefore, peri-infarction ischemia may be more arrhythmogenic than ischemia at a distance from the infarct zone, but this is not known. METHODS AND RESULTS: Forty-two anesthetized open-chest pigs with a 1-month-old myocardial infarction induced by permanent ligature of the distal left anterior descending coronary artery (LAD) underwent a coronary reocclusion at either the proximal LAD (group 1, peri-infarction ischemia, n=21) or at the circumflex coronary artery (group 2, ischemia at a distance, n=21). Ventricular arrhythmias were analyzed during 60 minutes of coronary reocclusion and during programmed electrical stimulation. Infarct size was measured, and underperfusion at the occluded area was estimated by recording 99mTc-tetrofosmin activity. Weights of acute ischemic (23+/-9 versus 21+/-9 g) and healed infarction (10+/-6 versus 10+/-3 g), baseline LV pressure and peak of LV dP/dt, and radiotracer activity at the occluded area (3+/-2% versus 5+/-2% of normal tissue) were comparable between the two groups. Compared with group 2, group 1 showed more ventricular premature beats (median, 136 versus 59; P=.008), a higher incidence of spontaneous sustained ventricular tachycardia (57% versus 19%, P=.02) and ventricular fibrillation (76% versus 47%, P=.05), and greater electrical inducibility of sustained ventricular tachycardia (65% versus 28%, P=.03) but comparable induction of ventricular fibrillation. CONCLUSIONS: Ischemia superimposed at the border of a 1-month-old myocardial infarction is more arrhythmogenic than ischemia at a distance from the infarct zone in swine. Data suggest the presence of electrophysiological instability at the peri-infarction zone.

Animals↗
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

[Human and technical resources of arrhythmia units in Spain in 1995].

The results of the Spanish registry for electrophysiology and arrhythmias activity are presented. A questionnaire was sent to all of the Arrhythmia Units in Spain, directed to their human and technical resources, and activity. The questionnaire was designed by the Section of electrophysiology and Arrhythmias of the Spanish. Society of Cardiology. The existence of an arrhythmia Unit, as an autonomous center, was recognized in 26 cases, at the end of 1995. In 13 centers there was no Arrhythmia Unit, but 11 wanted to develop one and in 2 it was not considered. Seven centers expected to create an Arrhythmia Unit during 1996. The first Arrhythmia Unit in spain was created in 1979. We have considered as a basic requirement the functional existence of a specific cardiac electrophysiological laboratory. Only 34 hospitals already have a Laboratory and 5 are waiting for the development of one. In 21 hospitals there are cardiologists particularly dedicated to electrophysiology, the number varies between 1 and 3 in each hospital. Radiofrequency catheter ablation is now considered the technique of choice for the treatment of most cardiac arrhythmias. This technique is currently being performed in Spain in 29 Hospitals and an additional 4 are expected to be able to perform it in the near future. Twenty-five hospitals implant automatic defibrillators, and the mean defibrillators implanted per hospital and year is 9.8 +/- 10.1.

Arrhythmias, Cardiac↗