Biomedical subjects
Publications and source records attributed to A Piwnica.
We describe a balloon catheter designed for perfusing cardioplegic solution retrograde through the coronary sinus during cardiac surgical procedures. Emphasis is placed on features that increase both the safety and the effectiveness of this alternative means of delivering cardioplegic solution.
This study assesses the long-term results of emergency surgical repair of postinfarction ventricular septal defect (VSD). The cases of 28 patients surviving early operative closure of septal rupture (within 1 day to 20 days of the infarction) were reviewed. Only 1 had concomitant coronary artery bypass grafting. Follow-up ranged from 7 to 16 years with an average of 9 years. Four patients were lost to follow-up. There were 4 late deaths, 2 of which were of cardiac origin. One was due to congestive heart failure and 1 to arrhythmia, 1 and 6 years after operation, respectively. Of the remaining 20 patients, 8 are in New York Heart Association Functional Class I and 12 are in Class II. Two patients underwent reoperation, 1 for a left ventricular false aneurysm 5 years postoperatively and the other for unstable angina 10 years postoperatively. Both had an uneventful postoperative course. Only 2 patients had late coronary events (1, nonfatal myocardial infarction; 1, unstable angina). We conclude that aggressive management of postinfarction VSD is fully justified in view of the long-term survival and functional palliation that can be anticipated for operative survivors. We advocate that preoperative coronary artery angiography and subsequent bypass grafting be performed on a selective rather than routine basis.
The cardiac myosin phenotype, an important determinant of myocardial contractility, is modified by chronic increases in hemodynamic load. To quantify the proportion of atrial alpha-myosin heavy chain in various types of left atrial overload and to assess the possible relation between this proportion and atrial size, 34 patients were studied, 4 with Wolff-Parkinson-White syndrome, 29 with various types of mitral valve dysfunction and 1 with an atrial septal defect. Four normal autopsy hearts were also studied. The proportion of alpha-myosin heavy chain among total (alpha plus beta) myosin heavy chains was determined in each atrial sample, using an enzyme-linked immunosorbent assay. The size of the left atrium was assessed by one- and two-dimensional echocardiography. Alpha-myosin heavy chain was the main isoform present in the normal atria (85.5 +/- 9% of total myosin heavy chains). Patients with pure tight mitral stenosis (n = 9), mitral stenosis plus mild regurgitation (n = 8) and severe mitral regurgitation (n = 8), who had a higher indexed left atrial transverse diameter than those with Wolff-Parkinson-White syndrome (33 +/- 6, 39 +/- 10 and 46 +/- 5 versus 19.5 +/- 2 mm/m2, p less than 0.01, p less than 0.001 and p less than 0.001, respectively), also demonstrated a much smaller percent of alpha-myosin heavy chain content (28 +/- 20, 23.5 +/- 13 and 12 +/- 10 versus 58 +/- 18%, p less than 0.01, p less than 0.01 and p less than 0.001, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
Inadequate atrial hypothermia and subsequent ischemic injury have been recognized as the major causes of supraventricular arrhythmias (SVAs) and conduction defects following cold chemical cardioplegia. This study was designed to assess the effects of right atrial cooling (15 degrees-20 degrees C) during cardioplegic arrest upon the incidence of postoperative SVAs and conduction defects in 40 consecutive patients undergoing isolated aortic valve replacement. Atrial preservation was ensured by combining systemic (24 degrees C) and topical hypothermia with snared double caval cannulation during arrest. Myocardial temperatures in the right atrial septum and anterior wall of the right ventricle were recorded before and after each cardioplegic infusion and upon release of caval tapes. Postoperatively, the incidence of SVAs and conduction defects was assessed by continuous rhythm monitoring, bipolar atrial electrograms and, in ten patients, 24-h Holter recordings during the first postoperative day. With the venae cavae snared, temperatures in the right atrial septum were not significantly different from those measured simultaneously in the right ventricle. Release of caval tapes resulted in right atrial temperatures increasing to systemic temperature (from 17.1 +/- 2.9 degrees C to 25.9 +/- 5.6 degrees C [m +/- SD]; P less than 0.01). Atrial rewarming between cardioplegic infusions did not exceed 2.9 degrees +/- 3.2 degrees C. Postoperatively, four patients (10%) developed sustained atrial fibrillation. One additional patient had a single episode of paroxysmal atrial fibrillation and two patients experienced asymptomatic episodes of junctional rhythm.(ABSTRACT TRUNCATED AT 250 WORDS)
We implanted the automatic implantable defibrillator model B (AID-B) in 11 patients (pts). Seven pts had coronary disease with sustained VT, and/or VF. Two had syncopal VT due to primary cardiomyopathy, and two pts had syncopal torsades de pointes (Tdp) without cardiac disease (1 long QT syndrome). These arrhythmias occurred despite antiarrhythmic drugs or beta blockers. Four pts had implanted: an epicardial patch by thoracotomy, an intra-atrial string electrode by the jugular vein, then AID-B by abdominal route. In 7 pts, subcostal approach was used, for implanting simultaneously 2 epicardial patches and the AID-B itself. During the operation, VT, Tdp and/or VF were induced in all pts by 50 Hz alternating current. The defibrillation threshold (DT) between atrial catheter and epicardial patch was less than 15 J in 4 pts, and greater than 25 J in two, requiring a larger patch in 1, and replacement of atrial electrode by another patch in the 2nd pt to obtain a DT less than 20 J. In the 6 pts implanted with 2 patches, DT was always less than 25 J. In 3 pts, DT was markedly higher for VF (25 J) than for VT (less than 15 J). One pt died from pulmonary embolism, another died after 3 years, before replacement of a failing battery, and a third died from progressive congestive heart failure, 6 months later. Eight pts are alive with a follow-up greater than 6 months. Local aseptic reactions obliged a removal of the implant in 2 pts operated by bifocal approach, and none when the subcostal route was used.(ABSTRACT TRUNCATED AT 250 WORDS)
The hydroxyl radical is one of the most damaging oxygen metabolites that are thought to be produced during ischemia and reperfusion of cardiac tissue. Therefore, we used the isolated, isovolumetric, buffer-perfused rat heart preparation of cardioplegic arrest to assess the effects of interventions targeted at inhibiting production of the hydroxyl radical by decreasing either the availability of one of its precursors (hydrogen peroxide) or that of the metal catalyst (ferric iron) involved in the radical formation. Sixty hearts were studied and, except for nonischemic controls, were subjected to 3 hr of hypothermic (15 degrees to 18 degrees C) cardioplegic arrest, followed by 45 min of reperfusion. The following interventions were tested: pretreatment with peroxidase, a scavenger of hydrogen peroxide, pretreatment with a combination of peroxidase and the iron chelator deferoxamine, pretreatment with peroxidase followed by supplementation of the cardioplegic solution with deferoxamine, and supplementation of the cardioplegic solution with deferoxamine without preischemic enzymatic treatment. Based on comparisons of postreperfusion pressure development, maximal ventricular dP/dt, left ventricular compliance, and coronary flow, deferoxamine-containing cardioplegic solution alone afforded the best myocardial protection. This may be due to the ability of deferoxamine to act both as an iron chelator and as a direct scavenger of superoxide anion, an activated oxygen species that participates in hydroxyl radical formation. This study confirms that an important component of the cardiac damage sustained during global ischemia and reperfusion may involve injury caused by the hydroxyl radical. Furthermore, our results point out the potential therapeutic usefulness of deferoxamine in the context of cardioplegic protection during open-heart procedures.
Between October 1982 and May 1986, 12 patients were implanted with an automatic defibrillator AID-B; 7 had coronary artery disease, 2 had dilated cardiomyopathies and 3 had torsades de pointe with or without long QT intervals. Five patients had a thoracic approach with a left ventricular patch and implantation of a right atrial endocavitary electrode. Thereafter a subcostal approach was used with 2 patch electrodes. Two of the first 5 patients rejected the device, but this complication was not observed in the remaining 7 cases. The threshold of defibrillation was greater than 25 joules in 1 case out of 5 with a patch and endocavitary electrode. This threshold was less than 25 joules in all patients with 2 patch electrodes. The AID-B was triggered in less than 20 seconds. One patient died of pulmonary embolism 8 days after implantation; 2 others had a temporary aggravation of their arrhythmias. There were no cases of inappropriate activation of the AID-B device during follow up: 5 patients had no arrhythmia or defibrillation. The 6 others had 2 to 35 defibrillations with documented arrhythmias before or after defibrillation. One patient suffered a sudden death after exhaustion of the device which had functioned on two occasions but had not been replaced for economic reasons. The technique of implantation has been simplified, so limiting local complications. This device is reliable and represents an effective palliative treatment of sudden death due to ventricular arrhythmias.
The authors report their experience of 28 cases of the Wolff-Parkinson-White (WPW) syndrome treated by surgery. Four patients had multiple accessory pathways; of the 32 bundles of Kent detected, 16 were in the postero-septal region. Surgery, performed under cardio-pulmonary bypass after epicardial mapping, consisted in atrioventricular disconnection using no special physical agent. With the exception of 2 cases, the left lateral accessory pathways were operated using a classical left intraatrial approach whereas in the right lateral and septal forms the main procedure of dissection of the right atrioventricular groove was carried out by an epicardial approach. There was one operative death due to haemodynamic and haemorrhagic problems in a top class athlete with two bundles of Kent, the interruption of which required two consecutive bypass procedures. In the 27 survivors, 29 of the 30 accessory pathways were successfully interrupted (96 p. 100). The only failure occurred in a patient with two bundles of Kent. On the other hand, in 2 patients, complete atrioventricular block was successfully obtained by surgical section of the His bundle during the same procedure in one case, and by postoperative catheter ablation in the other case in which surgery had failed. There were no cases of accidental permanent atrioventricular block. The results in this series confirm the value of surgery in the treatment of the WPW syndrome, especially in the septal forms which are reputed to be the most difficult but in which the approach is greatly simplified by the initial dissection of the tricuspid ring by an epicardial approach.(ABSTRACT TRUNCATED AT 250 WORDS)
Major heparin-induced thrombocytopaenia (HIT) is a condition which is feared more for its thrombotic complications than for the risk of haemorrhage. The platelet count is part of routine surveillance of patients receiving this treatment which must be withdrawn if HIT occurs. The use of heparin remains essential for cardio-pulmonary bypass surgery. There are two possible scenarios: The thrombocytopaenia occurs in the postoperative period: the standard heparin may be relayed by oral anti-vitamin K anticoagulants, platelet antiaggregant drugs or by low molecular weight heparin (LMWH). The diagnosis of HIT is made before surgery: three therapeutic attitudes are discussed with respect to the urgency of surgery: surgery is deferred for 6 to 8 weeks to allow the platelet count to return to normal and the responsible circulating antibody to disappear; the use of LMWH providing the tests of platelet aggregation are negative with this product; in addition, there are other problems specific to their use in cardiopulmonary bypass to be considered; blood exchange at the beginning of cardiopulmonary bypass to eliminate the circulating factor responsible and so allow the use of standard heparin during and after the operation: this is the only possible solution in cases with in vitro aggregant activity of LMWH.
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There is at this point a large number of experimental studies suggesting that oxygen free radicals play a major role in the pathogenesis of the myocardial lesions observed during the sequence ischemia-revascularization. Today, it is stressed upon the role of leucocytes as well as iron as major mediators in triggering and maintaining free radicals generating reactions which lead to a lipidic peroxidation of the membranes. It is probable, and anyway desirable, that these converging studies result, in the very near future, in the development of free radicals traps which are clinically usable. Such a development is still undissociable from the identification of specific markers of radicals lesions in the tissues, which is a mandatory condition for a serious evaluation of the procedures likely to bring under control the harmful effects of these unstable oxygen derivatives and therefore complete the arsenal of anti-ischemic treatments.
The technique of retrograde coronary sinus perfusion of a cardioplegic solution in cardiac surgery under cardiopulmonary bypass is described with emphasis on the characteristics of a catheter specifically devised to improve the effectiveness and safety of this type of cardioplegia.
Oxygen free radicals are very unstable metabolites which are produced in abundant quantity during the reoxygenation of an ischemic organ. Oxidation, by these radicals, of the structural lipids of the membranes, is at the origin of cellular lesions all the more extensive as the ischemia, by itself, decreases the ischemic tissue content in "trapping" molecules which usually inactivate those free radicals. Thus, was introduced the concept of an exogenous supply of trappers intended to bring under control the production of radicals and consequently preserve the membrane integrity in the revascularized tissue. This review summarizes, in light of our experience, the results obtained with free radicals trappers in the scope of myocardial preservation, especially in cardiac surgery, and analyzes some of the problems that remain to be resolved before considering the clinical use of these trappers.
Refractory and recurrent ventricular tachycardias are a common cause of death after myocardial infarction. The occurrence of intraventricular re-entries can be prevented by a new surgical treatment based on encircling thermic exclusion. The Nd-YAG laser beam offers 2 major advantages over previous techniques: it acts rapidly with minimal myocardial damage and can even be used in patients with left ventricular dysfunction.
In an attempt to assess their respective values for purposes of drug monitoring, plasma, red blood cell, atrial, and ventricular concentrations of amiodarone and N-desethylamiodarone (NDA) were measured, in 50 surgical patients, after a single oral dose (30 mg/kg); hemodynamic changes were assessed also. Amiodarone concentration was lower in red blood cells than in plasma and in myocardium. A relationship was found between the red blood cell concentration and plasma or myocardial concentrations of amiodarone (r = 0.79 and r = 0.68, p less than 0.00001). Hemodynamic studies were available in 17 treated patients and 13 control subjects before and at the time of surgery. In control subjects, hemodynamics did not change with time and general anesthesia. Oral amiodarone decreased the cardiac index (p less than 0.05) and heart rate (p less than 0.001) without significant changes in arterial pressure, systemic vascular resistance, or stroke volume index. The increase in capillary wedge pressure was related to amiodarone or NDA plasma, myocardial, and red blood cell concentrations (for amiodarone: r = 0.61, p = 0.006; r = 0.69, p less than 0.001; and r = 0.53, p = 0.02, respectively). We concluded that oral amiodarone impairs hemodynamics and that measurement of the amiodarone plasma concentration rather than the red blood cell concentration is the easiest method of monitoring the drug. However, establishment of the clinical utility of drug monitoring during chronic administration of amiodarone needs further investigation.
Oxygen-derived free radicals play an important role in the myocardial injury associated with ischemia and reperfusion. This study was designed to assess whether the protection afforded by a K+ rich, Mg2+ rich cardioplegic solution could be enhanced by the addition of free radical scavengers acting at different levels of the radical generating pathway. Forty isolated isovolumic rat hearts were divided into five groups (n = 8). Four groups of hearts were subjected to 90 minutes of normothermic cardioplegic arrest followed by 45 minutes of reperfusion. Hearts were given an initial bolus of either unmodified cardioplegic solution or cardioplegic solution enriched with superoxide dismutase (200,000 U/L) reduced glutathione (0.1 mmol/L), or peroxidase (6,000 U/L). One group of hearts was aerobically perfused throughout the experimental protocol and served as nonischemic controls. Based on comparisons of postreperfusion ventricular pressure development, maximal ventricular dP/dt, left ventricular compliance and coronary flow, peroxidase-containing cardioplegic solution afforded the best myocardial protection, with values of these indicators not significantly different from those of nonischemic perfused control heart. Glutathione afforded protection slightly inferior to that of peroxidase but still markedly better than in groups receiving superoxide dismutase or unmodified cardioplegic solution. This study confirms that cardioplegic protection can be enhanced by the addition of free radical scavengers, in particular peroxidase.
This study assesses the ability of the free-radical scavenger peroxidase to enhance cardioplegic protection when given during or before myocardial ischemia. Forty-four isolated isovolumetric buffer-perfused rat hearts were studied. In a first series of experiments that consisted of three groups, hearts were subjected to 90 min of normothermic global ischemia followed by 45 min of reperfusion. One group received a crystalloid cardioplegic solution given as a single dose at the onset of arrest. A second group received cardioplegic solution supplemented with superoxide dismutase (200,000 U/liter), and a third group received cardioplegic solution supplemented with peroxidase (6000 U/liter). Based on comparisons of postreperfusion coronary flow, left ventricular developed pressure, maximum dP/dt, and diastolic pressure, we found that the best protection was provided by peroxidase-enriched cardioplegia. A second series of experiments was then undertaken to assess the effects of the latter enzyme given as a pretreatment. Hearts were subjected to 3 hr of global ischemia, during which myocardial protection was provided by hypothermia (15 degrees C) along with multidose cardioplegia. The treatment group was given peroxidase (10,000 U/liter) added to the perfusate fluid for 15 min before the onset of cardioplegic arrest without further enzyme supplementation during ischemia or reperfusion. Hearts perfused with standard buffer for an equal period of time served as controls. While the two groups demonstrated the same degree of postischemic increase in myocardial stiffness, peroxidase-pretreated hearts had a significantly better recovery of contractile indexes at 30 and 45 min of reflow.(ABSTRACT TRUNCATED AT 250 WORDS)
Between 1970 and 1979, 28 patients (18 men and 10 women, aged 46 to 76 years, average 62 years) with acute myocardial infarction complicated by septal rupture survived surgery performed during the acute phase. In the same period 62 patients were admitted to the Cardiology Department and were operated early for septal rupture complicating myocardial infarction. The site of infarction was the anterior wall in 22 cases and the posterior wall in 6 cases; septal rupture occurred on average after 4.2 days (range 1 to 10 days); 15 patients including 13 with cardiogenic shock underwent intraaortic balloon pumping for an average of 3:7 (range 1 to 11 days) before surgery; the operation performed after an average interval of 11 days consisted in direct suture of the defect in 3 cases and a patch repair in the other 25 cases, associated in all cases with infarctectomy and LAD coronary bypass grafting in 1 case. The immediate postoperative course was simple; three patients with residual shunts were not reoperated. Five to 14 years later, in 1984, 4 patients had been lost to follow-up; 4 patients had died, 2 of cardiac causes (LVF after 1 year and an arrhythmia after 4 years). Of the 20 survivors, 2 were successfully reoperated (1 coronary bypass after 10 years and 1 false aneurysm after 5 years). Only one patient had recurrent myocardial infarction. The quality and longevity of long-term survival encourage early surgery. The factors affecting long-term survival are discussed: correction of associated valvular defects, resifual shunts, conservation of left ventricular function and evaluation of the coronary circulation.(ABSTRACT TRUNCATED AT 250 WORDS)