Cardiologia
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- True double aortic lumen in tetralogy of Fallot.Publication . Marinho da Silva, A; Sá e Melo, A; Providência, LAIn an infant with tetralogy of Fallot submitted to angiographic study, a double aortic lumen was found. Although no particular complaints were related to the additional abnormality, we report this case to emphasize the possibility of occurrence of persistent embryonic fifth aortic arch.
- Haemodynamics during liver transplantation in familial amyloidotic polyneuropathy: study of the intraoperative cardiocirculatory data of 50 patientsPublication . Viana, JS; Bento, C; Vieira, H; Neves, S; Seco, C; Elvas, L; Coelho, L; Ferrão, J; Tomé, L; Perdigoto, R; Craveiro, AL; Providência, LA; Furtado, ALBACKGROUND: Circulatory instability frequently complicates liver transplantation for familial amyloidotic polyneuropathy (FAP) and may be a source of surgical morbidity and mortality. OBJECTIVE: To evaluate FAP intraoperative haemodynamic data and their relation to the duration of surgery, and need for anaesthetic drugs. RBC and sympathomimetic amines. SETTING: Clinical study during a four year period. PATIENTS (mean +/- SD): Group I included 50 consecutive FAP ATTR Met 30 recipients of first transplantation. Age was 35.3 +/- 7.1 years, neurological score 34.3 +/- 13 in 100 and time elapsed from first symptom 5.0 +/- 2.7 years. Group II (control), not different concerning age and sex, included 51 patients transplanted during the same period with other pathologies. METHOD: Anaesthetic protocol, monitoring and surgical techniques were similar in both groups. Data of the two groups were compared either by the Student's t-test or Fisher's exact test. RESULTS: Low values of systemic vascular resistance index were observed in both groups, with no differences between them. Systemic arterial pressures were usually lower in group I, because cardiac index and heart rate were also significantly lower, although within normal values. However, in group I, isoflurane (a vasodilator anaesthetic) was used during less time (p < 0.05) and in lower concentrations (p < 0.01) and phenylephrine was necessary in 26% of patients vs 0 patients in group II (p < 0.001). CONCLUSION: FAP patients presented a different intraoperative behaviour when compared to other patients submitted to liver transplantation. From a clinical point of view, the authors stress: 1--As a result of autonomic dysfunction, the administration of anaesthetic drugs to FAP patients always presents the risk of producing significant hypotension; even the use of ketamine does not prevent hypotension; 2--Safety is ensured by beat-to-beat surveillance of arterial pressures and the capacity to act immediately to support circulation; 3--These patients seem to be very sensitive to decreases in the pre-load; 4--Hypotension is also frequent with an adequate pre-load, usually as the result of low SVR; an infusion of a vasoconstrictor drug emerges as the most frequent treatment requested and our experience supports it as an effective one.
- Angiogenic growth factors: potential new treatment for acute myocardial infarction?Publication . Gonçalves, LIn models of hind-limb ischemia and progressive coronary artery occlusion, angiogenic growth factor proteins and genes expressing growth factors have been shown to induce the development of collateral vessels and remodeling of existing collaterals. The therapeutic potential of growth factors in the setting of acute myocardial infarction may be related to non-angiogenic properties of growth factors as well, and is the focus of this review.
- Pacing biventricular: experiência inicialPublication . Pires, R; Monteiro, P; Cristovão, J; Antunes, A; Ventura, M; Costa, M; Ermida, P; Providência, LAINTRODUCTION: Biventricular pacing has been studied for the treatment of chronic heart failure (CHF). This technique seems to be able to improve symptoms and exercise tolerance, in patients with advanced CHF and prolonged QRS duration. OBJECTIVE: To present our experience with biventricular pacing in the management of severe CHF. METHODS: Between June 2000 and March 2001, 8 patients with dilated cardiomyopathy and left bundle branch block (LBBB) were selected for transvenous biventricular pacing system implantation. Mean age: 54.12 +/- 16.8 years; 5 males. The etiology was: idiopathic in 6 cases; operated congenital heart disease in 1, and ischemic in the other. Despite tailored treatment of CHF (with all patients taking diuretics and angiotensin-converting enzyme inhibitors), 7 patients remained in NYHA class III and 1 in IV. The quality of life score (assessed by the "Minnesota living with heart failure questionnaire") was 62.25 +/- 11.29. Seven patients had sinus rhythm and only one chronic atrial fibrillation; mean PQ duration--220 +/- 76.37 ms; mean QRS duration--168.75 +/- 20.31 ms. RESULTS: Implant failure, due to coronary sinus dissection and to excessive fluoroscopy time, with no coronary sinus catheterization, occurred in 2 cases (success rate: 75%). Implant data: mean implant procedure duration: 122.5 +/- 47.82 min; mean fluoroscopy time: 35.66 +/- 22.06 min; QRS duration, after implant: 133.33 +/- 15.05 ms. Left ventricular lead final position: anterolateral in 2 patients and lateral in 4. Pacing thresholds: biventricular--1.36 +/- 0.6 V; right ventricle--0.28 +/- 0.04 V; right atrium--0.32 +/- 0.08 V. Pacing impedance (left ventricle): 1013.33 +/- 147.87 omega. Follow-up (1st and 3rd month): one patient died, suddenly, 15 days after the procedure. In the others, an improvement in the quality of life index and functional class was found. These results were independent of echocardiography data. There were no significant differences in the pacing threshold and impedance during the follow-up. CONCLUSIONS: Patients with advanced CHF and widened QRS benefited from biventricular stimulation, in which improvement on the clinical status was evident.
- Impacto do Carvedilol Sobre O Dano Mitocondrial Induzido Por Hipoxantina/xantina Oxidase: Que Papel Na Isquemia e Reperfusão do Miocárdio?Publication . Oliveira, PJ; Rolo, AP; Monteiro, P; Gonçalves, L; Palmeira, CM; Moreno, AJOBJECTIVES: The cardioprotective effects of carvedilol (CV) may be explained in part by interactions with heart mitochondria. The objective of this work was to study the protection afforded by CV against oxidative stress induced in isolated heart mitochondria by hypoxanthine and xanthine oxidase (HX/XO), a well-known source of reactive oxygen species (ROS) in the cardiovascular system. METHODS: Mitochondria were isolated from Wistar rat hearts (n = 8) and incubated with HX/XO in the presence and in the absence of calcium. Several methods were used to assess the protection afforded by CV: evaluation of mitochondrial volume changes (by measuring changes in the optical density of the mitochondrial suspension), calcium uptake and release (with a fluorescent probe, Calcium Green 5-N) and mitochondrial respiration (with a Clark-type oxygen electrode). RESULTS: CV decreased mitochondrial damage associated with ROS production by HX and XO, as verified by the reduction of mitochondrial swelling and increase in mitochondrial calcium uptake. In the presence of HX and XO, CV also ameliorated mitochondrial respiration in the active phosphorylation state and prevented decrease in the respiratory control ratio (p < 0.05) and in mitochondrial phosphorylative efficiency (p < 0.001). CONCLUSIONS: The data indicate that CV partly protected heart mitochondria from oxidative damage induced by HX and XO, which may be useful during myocardial ischemia and reperfusion. It is also suggested that mitochondria may be a priority target for the protective action of some compounds.
- Carvedilol: Relação Entre A Actividade Antioxidante e Inibição da Transição de Permeabilidade MitocondrialPublication . Oliveira, PJ; Esteves, T; Rolo, AP; Monteiro, P; Gonçalves, L; Palmeira, CM; Moreno, AJOBJECTIVES: The mitochondrial permeability transition (MPT) is an event related to severe oxidative stress (for example, during myocardial ischemia and reperfusion) and excessive mitochondrial calcium accumulation, also being implicated in cell death. In this study, we compared the effect of carvedilol on the cardiac MPT induced by calcium and phosphate (Ca/Pi) and calcium/carboxyatractyloside (Ca/Catr). Oxidative stress plays a major role in MPT induction by Ca/Pi, leading to the oxidation of protein thiol groups, in contrast with Ca/Catr, where such oxidation is secondary to MPT induction and is not caused by oxidative stress. MATERIALS AND METHODS: Mitochondria were isolated from rat hearts and parameters related to MPT induction were evaluated (n = 5 for each inducer): mitochondrial swelling and oxidation of protein thiol groups (both measured by spectrophotometry). RESULTS: Using Ca/Pi, carvedilol protected mitochondria from MPT induction, particularly in its high conductance form. Its effect was demonstrated by analyzing the decrease in mitochondrial swelling amplitude. Simultaneously, we observed inhibition of protein thiol group oxidation (p < 0.001). By contrast, carvedilol did not show any protective effect with Ca/Catr. CONCLUSIONS: Carvedilol was only effective against the MPT when the oxidation of protein thiol groups was the cause and not the consequence of the MPT phenomenon. The results clearly show that during myocardial aggressions (ischemia and reperfusion, for example), the protective effect of carvedilol is primarily due to an antioxidant mechanism, inhibiting the production and effects of reactive oxygen species.
- Carvedilol improves energy production during acute global myocardial ischaemiaPublication . Monteiro, P; Duarte, AI; Moreno, AJ; Gonçalves, L; Providência, LACardiac mitochondria may become dysfunctional during ischaemia, thus compromising cardiomyocyte function. Carvedilol is an alpha(1)/beta-adrenoceptor antagonist with antioxidant, neuroprotective, cardioprotective and vascularprotective properties, and is used to treat hypertension, myocardial ischaemia and congestive heart failure. However, its impact on mitochondrial function during acute prolonged ischaemia is unknown. We aimed to study the effect of carvedilol on cardiac mitochondrial function during acute ischaemia, using Wistar rat hearts perfused with a Langendorff system, and then submitted to ischaemia in the presence and absence of carvedilol. We determined the electrical potential of the mitochondrial membrane, O(2) consumption by the respiratory chain, energy charge and the activity of the mitochondrial respiratory chain complexes. In our model, carvedilol had a preferential action on phosphorylation, increasing the mitochondrial energy charge (0.76+/-0.03 vs. 0.65+/-0.01 arbitrary units; P<0.05) and decreasing the phosphorylation lag phase (28.64+/-4.23 vs. 62.4+/-11.63 s; P<0.05) during ischaemia. The larger amount of energy available allowed the preservation of the electrical potential (201.2+/-2.45 vs. 186.66+/-3.36 mV;P<0.05), thus improving mitochondrial function during acute prolonged ischaemia
- O Piruvato Melhora A Energética Mitocondrial Num Modelo Animal Ex-vivo de Isquemia Miocárdica GlobalPublication . Monteiro, P; Duarte, AI; Moreno, AJ; Gonçalves, L; Providência, LAPyruvate is an energy substrate with known cardioprotective activity. We know now that this is due not only to its antioxidant activity, but also to its reduction of intracellular acidosis, modulation of intracytosolic calcium and improvement of cardiomyocyte contractility. However, the role of cardiac mitochondria in such positive effects has only recently begun to be understood and the exact mechanisms of the effect of pyruvate on mitochondria are still largely unknown. Aiming to study the effect of pyruvate on cardiac mitochondrial function during acute ischemia, we used an ex-vivo animal model, perfused in a Langendorff system and then subjected to ischemia in the presence and absence of pyruvate. We evaluated the mitochondrial membrane electrical potential, the respiratory chain O2 consumption (and respiratory control ratio) and the energy charges generated with different energy substrates. We conclude that pyruvate has some effect on the mitochondrial oxidative system (by non-significantly improving the respiratory control ratio), but its main action is on the phosphorylation system, significantly decreasing the time taken to complete a phosphorylation cycle (lag phase) and improving ATP production (increase in energy charge), thus allowing better maintenance of mitochondrial membrane structure, with consequent improvement of the electrical potential after a phosphorylation cycle. These findings have enabled better understanding of the mechanisms behind pyruvate cytoprotection in ischemic cardiomyopathy, clearly highlighting the essential role of cardiac mitochondria in this process.
- Mitocôndria: que papel na isquémia, reperfusão e morte cerebral?Publication . Monteiro, P; Oliveira, PJ; Gonçalves, LRecent advances in the knowledge of the biochemical basis of myocardial ischemia have enabled a better understanding of the complex sequence of events occurring in ischemic cardiomyopathy, whatever its manifestations. This has clearly highlighted the important role played by cardiac mitochondria in these events. At first only associated with energy production, mitochondria have been clearly shown to have other important functions, like the maintenance of calcium homeostasis, as well as ischemic and non-ischemic preconditioning, and also modulation of cellular life and death. The aims of this review are twofold: firstly, to review the current knowledge on mitochondrial morphology and structure, and how these can be affected by ischemia and ischemia-reperfusion; and secondly, to summarize the role of cardiac mitochondria in cardioprotection and modulation of cell death mechanisms.
- O Carvedilol Protege Mitocôndrias Cardíacas Isquémicas de Lesões Induzidas Por Stress OxidativoPublication . Carreira, R; Duarte, AI; Monteiro, P; Santos, MS; Rego, AC; Oliveira, CR; Gonçalves, L; Providência, LAIschemia negatively affects mitochondrial function by inducing the mitochondrial permeability transition (MPT). The MPT is triggered by oxidative stress, which occurs in mitochondria during ischemia as a result of diminished antioxidant defenses and increased reactive oxygen species production. It causes mitochondrial dysfunction and can ultimately lead to cell death. Therefore, drugs able to minimize mitochondrial damage induced by ischemia may prove to be clinically effective. We analyzed the effect of carvedilol, a beta-blocker with antioxidant properties, on mitochondrial dysfunction. Carvedilol decreased levels of TBARS (thiobarbituric acid reactive substances), an indicator of oxidative stress, which is consistent with its antioxidant properties. Regarding cell death by apoptosis, although ischemia did increase caspase-8-like activity, there were no changes in caspase-3-like activity, which is activated downstream of caspase-8; this may indicate that the apoptotic cascade is not activated by 60 minutes of ischemia. We conclude that carvedilol protects ischemic mitochondria by preventing oxidative mitochondrial damage, and, by so doing, it may also inhibit the formation of the MPT pore.