Reduction of the pace polarization artefact for capture detection applications by a tri-phasic stimulation pulse.

This study investigated the ability to minimize pace polarization artefacts (PPA) by adjusting the post-stimulus pulse duration of a tri-phasic stimulation pulse. Adjustment of the stimulation pulse was enabled by downloading special study software into an already implanted pacemaker. Tests were performed in a total of 296 atrial leads and 311 ventricular leads. Both chronic and acute leads were included in the study. Statistically significant differences were found in the initial PPA (without any adjustment of the stimulus pulse) between atrial and ventricular leads. In addition, significant differences were observed among various lead models with respect to changes over time in the initial ventricular PPA. Successful PPA reduction was defined as a reduction of the PPA below 0.5 mV for atrial leads and below 1 mV for ventricular leads. Results show a success rate for ventricular and atrial PPA reduction of 97.8% and 98.7%, respectively. Threshold tests showed that after reduction of the PPA loss of ventricular capture can be reliably detected. However, atrial threshold tests showed many false positive evoked response detections. In addition, unexpectedly high evoked response amplitudes were observed in the atrium after reduction of the PPA. Results from additional measurements suggest that these high atrial evoked response amplitudes come from the influence of the input filter of the pacemaker.

Distribution of conjugated linoleic acid and metabolites in different lipid fractions in the rat liver.

Conjugated linoleic acid (CLA) is known to provide certain health benefits in experimental animal models. The major CLA isomer in food is c 9,t11-CLA. A primary objective of this study was to investigate the uptake of c 9,t11-CLA and its downstream metabolites into various lipid fractions in the liver of rats fed either a high or low CLA diet (containing 0.1 or 0.8 g CLA/100 g diet, respectively). As expected, the levels of all conjugated diene (CD) fatty acids (CD 18:2 + CD 18:3 + CD 20:3 + CD 20:4) were elevated about 8-fold in the high CLA diet group. However, there was no change in the distribution of CLA and CLA metabolites into various lipid fractions due to CLA intake. Unlike linoleic acid or gamma-linolenic acid, which were distributed mainly in phospholipids, CD 18:2, CD 18:3, and CD 20:3 were incorporated primarily in neutral lipid. Furthermore, the incorporation of all nonconjugated unsaturated fatty acids was not perturbed by CLA. Regardless of the level of CLA in the diet, CD 20:4 was predominantly enriched in phosphatidylserine and phosphatidylinositol. In contrast, arachidonic acid was primarily enriched in phosphatidylcholine and less so in phosphatidylethanolamine. The above findings may have potential implication regarding the role of CLA in modulating eicosanoid metabolism.

[Programmed left ventricular stimulation in non-sustained ventricular arrhythmias]. / La stimulation ventriculaire programmée dans les arythmies ventricularies non soutenues.

The presence of nonsustained ventricular arrhythmia (NSVA) is an independent factor of sudden rhythmic death. The primary objective of our study was to evaluate the correlation between inducibility during programmed ventricular stimulation (PVS) and the presence of ventricular late potentials, the ejection fraction, the grade of arrhythmia, and the underlying cardiopathy. The secondary objective was to evaluate the interest of PVS in patients with NSVA. Ninety eight patients with NSVA have been tested by PVS and 14 were inducible. During the mean follow up of 24 months, 8 patients died, 3 of them suddenly. A significative statistical correlation was found between ventricular late potentials and inducibility (negative predictive value = 91%; p = 0.03). No correlation was found between the ejection fraction, the grade of arrhythmia, the cardiopathy and inducibility. In patients with ischaemic cardiopathy, PVS has allowed to identify a subgroup of patients with high risk of sudden death. In this subgroup, serial PVS for drug testing has contributed to choose the therapeutic regimen supposed to be more effective for prevention of fatal arrhythmia. Multiple factors explain sudden death, even though the initial treatment has been chosen by electrophysiologic studies. For non inducible patients, empiric treatment is not proven to be reliable, and the best therapeutic regimen is still unidentified, especially in the subgroup of patients with low ejection fraction. In this subgroup, the implantable cardioverter defibrillator vives better protection against sudden rhythmic death.

Randomized comparison of two targets in typical atrial flutter ablation.

Typical atrial flutter ablation has become anatomically guided to 2 separate sites within the isthmus at the inferior right atrium: (1) between the inferior vena cava and the tricuspid annulus (anterior side of the isthmus [A]), (2) between the eustachian crest, the coronary sinus ostium and tricuspid annulus (posterior side of the isthmus [P]). We prospectively compared ablation results at these sites in 72 consecutive patients. Patients were randomized in group P or A according to the initial target site. If ablation failed at 1 site after 15 radiofrequency (RF) pulses, the other side of the isthmus was targeted. Before 15 RF pulses, complete bidirectional isthmus block was achieved in 30 of 36 group A patients and in 25 of 36 group P patients, with similar mean RF pulses number, procedure time, and fluoroscopy time. After shifting to the other target, success was finally obtained at P in 2 of 6 group A patients, and at A in 8 of 11 group P patients before a maximum of 30 RF pulses. Among successful patients, number of RF pulses, procedure time, and fluoroscopy time were significantly lower in group A (7.2 +/- 5.4 vs 11.0 +/- 8.1 pulses, p = 0.03; 131 +/- 44 vs 163 +/- 66 minutes, p = 0.03; 31 +/- 19 vs 46 +/- 24 minutes, p = 0.01, respectively). Impairment of atrioventricular (AV) nodal conduction occurred in 5 patients only during ablation at P. AV block was transient in 4 patients and permanent in 1. Although atrial flutter ablation is equally effective at P and A, success seems easier to obtain when A is first targeted. Ablation at P is associated with a significant risk of AV block.

Iodine-123-metaiodobenzylguanidine SPECT of regional cardiac adrenergic denervation in Brugada syndrome.

We present the case of 44-yr-old man who presented syncope with ventricular tachycardia in the setting of Brugada syndrome. In addition to the electrocardiographic evidence of the syndrome and the absence of apparent structural heart disease, clear defects of myocardial neuronal metaiodobenzylguanidine (MIBG) uptake on MIBG SPECT imaging also were found in inferior, apical and septal walls. Thallium-201 SPECT distribution was homogeneous along the left ventricle. Thus, cardiac MIBG scintigraphy provides information about left ventricular dysinnervation in a patient with Brugada syndrome, enhancing the clinical utility of myocardial MIBG SPECT imaging in life-threatening ventricular arrhythmias.

[Value of cardiac scintigraphy with I123 meta-iodobenzylguanidine in congestive heart failure. A review]. / Valeur de la scintigraphie cardiaque a la 123I-méta-iodo-benzylguanidine dans l'insuffisance cardiaque congestive. Mise au point.

Heart failure is accompanied by major disturbances of the functioning of the sympathetic nervous system: global overactivation and local modifications of the adrenergic system. 123I-MIBG cardiac scintigraphy is an isotope technique investigating presynaptic adrenergic function. The cardiac uptake of MIBG is decreased during heart failure, reflecting a reduction of norepinephrine reuptake by cardiac presynaptic nerve endings. Alteration of presynaptic function occurs early and plays an important role in the pathogenesis of the deterioration of heart failure. 123I-MIBG cardiac scintigraphy allows in vivo assessment of the myocardial adrenergic reserves of patients with congestive heart failure. It should be proposed in all patients with severe ventricular dysfunction to help define the indications for heart transplantation.

[Effects of temporary dual-chamber cardiac pacing in refractory cardiac failure]. / Effets de la stimulation cardiaque double chambre temporaire dans l'insuffisance cardiaque réfractaire.

The authors studied 18 patients (15 men, 3 women) with an average age of 67 +/- 8 years with refractory cardiac failure. In order to determine the potential of pacing to raise cardiac output in severe cardiac failure. The average ejection fraction was 26 +/- 6.5%. All patients were in sinus rhythm:resting cardiac output was 3.35 l/min. Two temporary pacing catheters were positioned in the right atrium and at the apex of the right ventricle for dual-chamber mode pacing triggered by the spontaneous P waves. Changes in cardiac output were measured by Doppler echocardiography at different values of atrioventricular delay. Patients were considered to be responders if their cardiac outputs rose by 15%. In 7 patients meeting this criterion, the average increase in cardiac output was 27% (2.99 +/- 0.7 to 3.81 +/- 0.86 l/mn; p < 0.01); all had dilated cardiomyopathies with left bundle branch block and the optimal AV delay was 103 +/- 21 ms (80-140 ms); the duration of diastolic filling increased from 212 +/- 98 to 292 +/- 116 ms (p = 0.02). In the non-responding group (11 patients with an increase of cardiac output of only 3.6 +/- 0.09 to 3.9 +/- 0.92 l/mn; p < 0.01), the underlying disease process was mainly ischaemic. Two predictive factors of efficacy of dual-chamber pacing were identified: a short ventricular filling period (29 +/- 8% of the RR interval in the responders vs 44 +/- 9% in the non-responders; p < 0.01) and the presence of 1st degree atrioventricular block. Dual-chamber pacing could be a valuable method of increasing resting cardiac outputs in a selected group of patients with severe, refractory, cardiac failure.

[Cardiac transplantation. Evaluation of a consecutive series of 75 grafts]. / Transplantation cardiaque. Bilan d'une série consécutive de 75 greffes.

OBJECTIVES: The global results of various series of heart transplantation (HT) are essential to assess the life expectancy provided by this technique. Due to the increasing graft shortage, it appears essential to very strictly candidates for HT. METHODS: From March 8, 1989 to December 7, 1994, 75 orthotopic Hts were performed in 62 men and 12 women (1 case of retransplantation). The mean age was 47.46 +/- 15.02 years (range: 2.5-66 years). Four patients were younger than 10 years and 22 were older than 60 years. Our series included more cases of ischaemic heart disease (36) than dilated cardiomyopathies (33), with a history of cardiac surgery in almost one quarter (20) of patients with ischaemic heart disease. RESULTS: The immediate postoperative survival rate was 94.7% with 3 deaths attributable to refractory pulmonary hypertension associated with graft failure and one death related to postoperative tamponade. Five other patients died during the following 3 months, increasing the mean global survival to 88%. After a mean follow-up of 2.1 years (maximum 5.8 years), the actuarial 5-year survival rate was 56.8%. Eleven patients died between 4 and 38 months (mean: 18.2 months). Two deaths were due to cancers, 4 were due to septicaemia, another 4 were due to rejection and finally 1 was due to meningeal haemorrhage. The frequency (19) of reoperations for clot removal was due to the large number of patients with a history of previous heart surgery (20). CONCLUSION: Strict recipient selection, possibly based on 123I-MIBG scintigraphy, the use of pulsatile circulatory assistance systems, improved CMV, morphometry and donor-recipient age matching, should optimize the results of a technique, whose efficacy is confirmed in this series.

[Proarrhythmic effects of anti-arrhythmia agents]. / Les effets proarythmiques des médicaments antiarythmiques.

Antiarrhythmic medications are widely used either at the ventricular or supraventricular level. However, those drugs can induce severe side effects. Actually, antiarrhythmic drugs are paradoxically able to favour the occurrence of new arrhythmias or aggravate the preexisting arrhythmia for which they were indicated. These proarrhythmic effects have been found in 10 to 20% of patients, as evidenced by literature. Moreover, the CAST study showed a significant increase in mortality in patients with non sustained ventricular arrhythmias after myocardial infarction who were treated with either flecainide or encainide, compared to the placebo group. This overmortality seems to be due, in large, to the proarrhythmic effects of antiarrhythmic drugs. Several mechanisms have been evoked, related to the type of antiarrhythmic drug and to the presenting arrhythmia: early post-depolarization due to slow calcium and sodium inward currents in the case of torsades de pointes, facilitation of intraventricular reentries in the case of class 1c antiarrhythmic drugs, facilitation of the ventricular response of atrial arrhythmias. These deleterious effects, that can be very serious, are unpredictable, not toxicity-related and all antiarrhythmic drugs are involved. Their detection appears to be difficult and is based upon ECG, Holter monitoring, treadmill test and possibly electrophysiologic study. The use of antiarrhythmic drugs requires the knowledge of their proarrhythmic effects, the analysis of the benefit-risk ratio--particularly if left ventricular function is impaired--and careful monitoring.

[Myocardial infarction and revascularization. Current indications]. / Infarctus du myocarde et revascularisation. Indications actuelles.

The physiopathologic role of thrombosis in the genesis of myocardial infarction, began to be suspected early in the 20th century but its logical treatment, thrombolysis, was first used on a large scale only ten years ago. Today, it is well established that short, middle and long-term mortality is correlated to coronary permeability, the delay in the revascularization treatment start-up, its efficacy, its swiftness of action, and to the maintaining of permeability following reperfusion. The importance of time elapse before reperfusion is obtained was demonstrated as early as 1986 by the GISSI study. According to this study, the administration of streptokinase (compared to a conventional treatment) reduced mortality at 21 days respectively by 47%, 23%, and 17%, depending on whether patients were treated within one hour, three hours, or between 3 and 6 hours following the onset of the painful symptoms. One of the major teachings of the GUSTO study, reported at the end of 1993, was the confirmation of the so-called "open artery" theory: mortality at 30 days was of 4.5% among patients whose coronary circulation was restored at the 90th minute, whatever thrombolytic treatment was used, compared to 8.9% when the coronary artery remained occluded. The value of aspirin in preserving coronary permeability following thrombolysis was demonstrated by the ISIS-2 study: mortality at 5 weeks was reduced by 23% in the group of patients randomised to receive only aspirin, while it was reduced by 25% in the group of patients randomised to be treated with streptokinase, and by 42% in the group randomised to receive both aspirin and streptokinase, compared to the group who received neither aspirin nor streptokinase. However, mortality during the first days following randomisation was identical among the groups, with or without aspirin, which suggested its action was rather one of prevention against reocclusion than one of accelerating dissolution of the thrombus. However, in spite of improved therapeutical protocols, a normal flow, which is the major criteria for a reduced mortality, is only obtained at the 90th minute in 54% of the patients who were administered the up-to-date treatment ie aspirin-accelerated t-PA-heparin in combination.(ABSTRACT TRUNCATED AT 400 WORDS)

[Endocarditis caused by Cardiobacterium hominis]. / Endocarditis à Cardiobacterium hominis.

The incidence of endocarditis due to Cardiobacterium hominis is probably underestimated because clinical presentations vary greatly and culture of this Gram negative germ is difficult. A 48-year-old man with a past history of post-streptococcic aortic regurgitation was hospitalized twice within 1 week for fever (38 degrees C) and junctional tachycardia which responded to amiodarone. Subsequently, infero-apical necrosis was documented. Based on the result of the laboratory tests, coronary embolism was suspected although 12 blood cultures were negative. The patient recovered well with a standard antibiotic treatment. Fifteen days later, the blood cultures revealed Cardiobacterium hominis. Antibiotic therapy was adapted and aortic valve replacement was programmed. Two months later the patient died from uncontrollable left heart failure. A 63-year-old man who had had mitral valve replacement 10 years earlier for Streptococcus mitis endocarditis was hospitalized for fever (38 degrees C) and a painful left calf. Phlebocavography eliminated deep vein thrombosis and a complete cardiac work-up was inconclusive. Endocarditis was suspected although blood cultures were negative. The patient was given oral penicillin and discharged after one week. Three months later, the patient was again febrile (38 degrees C) and suffered a cerebral vascular event. Fourteen days after blood sampling, cultures revealed Cardiobacterium hominis. The patient's haemodynamic status worsened and valve replacement with atrioplasty was performed. Outcome after 4 years follow-up has been favourable. Endocarditis due to Cardiobacterium hominis, a saprophitic germ of the upper airway and the female genital tract, has been reported in 64 cases in the literature. The clinical picture is often limited to fever and a heart murmur and laboratory tests show an accelerated erythrocyte sedimentation rate and hyperleukocytosis. Inflammatory type anaemia is often found due to the latency of the endocarditis. Complications are frequent and can be fatal due to massive pulmonary emboli, cerebral vascular events or irreversible heart failure. C. hominis is sensitive to amoxycillin and netilmicin. Surgical treatment of the valvulopathy is indicated.

[Subacute rupture of the free wall of the heart. Clinical echocardiographic and pathological aspects apropos of 10 cases]. / Ruptures subaiguës de la paroi libre du coeur. Aspects cliniques, échocardiographiques et anatomiques à propos de 10 cas.

Three distinct forms of rupture of the heart may be identified after myocardial infarction: sudden rupture with massive intrapericardial haemorrhage, and sudden death with clinical signs of electromechanical dissociation; rupture into the pericardium resulting in a false aneurysm, the treatment of which is surgical; subacute rupture which accounts for 30% of cases in which bleeding into the pericardium is slow and/or repeated. Over an 8 year period and in a series of 2,400 consecutive infarcts admitted to the intensive care unit, 10 cases of subacute rupture of the heart were diagnosed. They were 6 men and 4 women, with a mean age of 73.6 years. The clinical presentation was isolated chest pain in 5 cases, syncope alone in 2 cases and the association of pain and syncope in 3 cases. Six patients were in shock on admission. In two cases, shock developed after admission. The infarction was confirmed biologically by a significant elevation of creatinine kinase in 9 out of 10 cases. Transmural infarction was observed in 9 cases: the infarct was electrocardiographically non-transmural in 1 case. Emergency echocardiography showed pericardial effusion in all cases, usually moderate, but sometimes compressive with an intrapericardial echogenic mass suggesting a thrombus. Haemodynamic improvement was obtained by medication allowing cardiac catheterisation which showed adiastole in 3 cases. Coronary angiography was performed in 7 cases. In 5 of the 7 cases, apart from occlusion of the artery presumed to be responsible for the infarct, the coronary vessels were diffusely infiltrated without significant stenosis. Left ventriculography was performed in 7 cases. In 6 of the 7 cases regional akinesis was demonstrated: the 7th case showed dyskinesia of the anterior wall. In two cases, contrast medium was observed to fill the pericardium during ventriculography, indicating myocardial rupture. The diagnosis of subacute rupture, suggested by clinical and paraclinical (particularly echocardiography), was confirmed in 9 cases at surgery and in the 10th case at autopsy. Surgery consisted of repairing the rupture. In the last two cases, biological glue was used to reinforce the surgical repair. The clinical outcome was good after surgery in 6 cases with a follow-up of 5 months to 8 years. The diagnosis of subacute rupture should therefore be made on clinical and echocardiographic criteria, as these results suggest that surgery is often possible, with a good prognosis.

[Early clinical, electrocardiographic and biological criteria of reperfusion after intravenous fibrinolysis during the acute phase of myocardial infarction]. / Critères précoces, cliniques, électrocardiographiques, et biologiques de reperfusion après fibrinolyse intraveineuse à la phase aiguë de l'infarctus du myocarde.

Between May 1991 and February 1992, 31 consecutive patients were included in a prospective study, the aims of which were to determine the criteria of early coronary revascularisation after intravenous thrombolysis in the acute phase of myocardial infarction. The rise in serum myoglobin, the ST segment elevation, accelerated idioventricular rhythm and the evolution of chest pain were analysed. All patients underwent coronary angiography. Twenty-six were revascularized and 5 remained with coronary occlusion. Two types of serum myoglobin curves were demonstrated. Those with a sudden , decrease and a well defined peak in the first 4 hours were specific for revascularisation and easily identified (Group A: 16 patients). The graphs with a progressively rising slope to a peak after the 4th hour were observed in patients with coronary occlusion, but also in 10 patients with recanalized arteries (Group B). No significant difference was demonstrated with regards to the clinical and coronary angiographic parameters between patients in Group A and Group B. On the other hand, the time between the onset of chest pain and peak myoglobin was shorter in Group A (298 +/- 81 min) than in recanalised patients in Group B (380 +/- 54 min) (p < 0.05). The difference in the profile of the serum myoglobin could therefore reflect restoration of arterial flow in myocardial cells which had not suffered the same period of ischemia. ST segment elevation may increase, decrease of remain stable at 120 minutes in patients revascularised and those remaining occluded. In 9 patients, the ST elevation increased compared with the initial electrocardiogram .(ABSTRACT TRUNCATED AT 250 WORDS)

[Correlations between the different criteria of late potentials and results of programmed ventricular stimulation after myocardial infarction]. / Corrélation entre les différents critères de potentiels tardifs et les résultats de la stimulation ventriculaire programmée au décours de l'infarctus myocardique.

Five to ten per cent of survivors of acute myocardial infarction die within two years. The majority of these deaths are sudden and are attributed to a lethal ventricular arrhythmia. This is usually ventricular tachycardia degenerating to ventricular fibrillation. These post-infarction tachycardias are generally due to reentry. They require an anatomic arrhythmogenic substrate, a zone of delayed conduction. This can be detected as late potentials on signal averaged ECG. The triggering of a significant ventricular arrhythmia by ventricular stimulation is closely correlated to the occurrence of a severe ventricular arrhythmia in the months following infarction. Programmed ventricular stimulation could, therefore, help to identify patients requiring close follow-up and/or preventive antiarrhythmic therapy, but cannot be offered to all patients because of its invasive nature. Seventy nine post-infarction patients were studied prospectively. All underwent coronary angiography, signal averaging electrocardiography, and programmed ventricular stimulation at least 15 days after infarction. Fifty five patients had at least one criterion of late potentials (QRS duration > or = 110 ms and/or amplitude of the last 40 ms < 27 microV and/or duration of potentials of under 40 microV > 37 ms). Twenty four patients had no late potentials. The results of programmed stimulation were estimated to be positive when sustained or unsustained monomorphic ventricular tachycardia was triggered, and negative when ventricular fibrillation, ventricular flutter unsustained polymorphic ventricular tachycardia or no arrhythmia could be induced. Programmed ventricular pacing triggered 15 significant events, 17 unsustained polymorphic ventricular tachycardias, 13 ventricular flutters and 11 ventricular fibrillations. The exploration was negative in 23 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Detection of enteroviruses in endomyocardial biopsy by molecular approach.

Enteroviruses are considered to be the most common agents implicated in myocarditis and cardiomyopathy. Recent studies have suggested persistent enterovirus infection in chronic disease showing the presence of enteroviral RNA in the myocardium. We used gene amplification by PCR which can demonstrate directly the presence of enteroviral sequences in endomyocardial biopsies. The primers were chosen in the 5' non-coding region of the genome representing highly conserved sequences among enteroviruses and therefore allowed the amplification of the majority of enteroviruses. The hybridization of the amplified products was effected with specific general riboprobe derived from 5' non-coding sequences internal of the amplified fragments. The results include 105 patients distributed in 6 groups: 45 idiopathic dilated cardiomyopathies with 66.7%, 17 alcoholic cardiomyopathies with 52.9%, 10 myocarditis with 30%, 5 multifactorial cardiomyopathies with 40%, 5 patients with immunosuppressive therapy with 100%, and 23 control group without viral etiology with 39.1% positive samples. The study suggested a positive link between viral infection and cardiomyopathies, but did not allow a direct relation between enterovirus infection and idiopathic dilated cardiomyopathy to be established.

[Lyme's disease, a possible cause of isolated acute myocarditis]. / Maladie de Lyme, cause possible de myocardite aiguë isolée.

The frequency of cardiac lesion in patients with other signs of Lyme disease has been estimated at 8 percent. The usual manifestation of myocardial involvement is a varying degree of atrioventricular block or more diffuse signs of myocarditis. Autopsy or intramyocardial biopsy provides a histological diagnosis of myocarditis. Microscopy shows a diffuse lympho-plasmocytic infiltrate with presence of macrophages in the myocardium, associated with a varying number of necrotic myocytes. Structures resembling spirochetes have been found in some cases. Exceptionally, the cardiac lesion may be isolated, presenting as an acute atrioventricular block and/or an acute myocarditis; in such cases the diagnosis of cardiac lesion caused by Lyme disease is made on serological grounds. We report the case of a 30-year old man admitted for acute myocarditis which turned out to be totally regressive. Intramyocardial biopsy showed interstitial congestion associated with inflammatory lympho-histiocytic infiltrates and eosinophilic polymorphonuclears; the myocardial fibres in contact with these infiltrates appeared to be altered. The diagnosis of Lyme disease was subsequently confirmed by serological tests. Patients with myocarditis caused by Lyme disease must be treated with antibiotics. Recent reports have demonstrated the presence of spirochetes in the myocardium of patients with dilated cardiomyopathy, suggesting that the spirochete Borrelia burgdorferi might be associated with, or play a part in, the subsequent occurrence of dilated cardiomyopathy.

[Myocardial dissection in infarction of the right ventricle. Clinical echocardiographic and pathological aspects]. / La dissection myocardique dans l'infarctus du ventricule droit. Aspects cliniques, échocardiographiques et autopsiques.

Dissection of the inferior wall of the right ventricle during the acute phase of myocardial infarction with right ventricular involvement is a mechanical complication which has been recently identified, the diagnosis being almost exclusively post-mortem. The authors report the clinical, echocardiographic and pathological features of myocardial dissection in four patients. Between 1985 and 1988, the diagnosis of myocardial dissection was made by echocardiography in 4 patients aged 77 to 80 years, admitted to hospital for an acute inferior wall myocardial infarction. All 4 patients had signs of acute right ventricular failure indicating right ventricular necrosis and a loud systolic murmur at the left sternal border; 2 patients were in shock. The ECG showed signs of inferior wall infarction with, in 2 patients, electrical changes suggestive of right ventricular involvement. Echocardiography showed dissection of the inferior wall of the right ventricle as a pulsatile, echo-free space in the diaphragmatic wall of the right ventricle which appeared to obstruct right ventricular ejection in end systole to a variable degree. The outcome was fatal in all cases with death resulting from refractory myocardial failure. Pathological analysis confirmed biventricular inferior wall infarction also involving the posterior part of the interventricular system, the site of a small tear on the left side which communicated with a neo-cavity dissecting the RV posterior wall. The right coronary artery was totally occluded in all cases. The anatomical lesions were fully concordant with the echocardiographic data: the dissection filled with blood from the left ventricle at each systole creating a pulsatile space in the diaphragmatic wall of the ventricle obstructing ejection.

[Isolated right ventricular infarction of coronary origin. Three cases]. / Infarctus isolés du ventricule droit d'origine coronaire. Trois observations.

In a series of more than 700 patients admitted over a 2-year period to an intensive care unit, 3 patients with isolated right ventricular infarction were observed. At electrocardiography the condition was characterized by isolated ST elevation in the anterior precordial leads. Infarction was due to obstruction of a right marginal coronary artery in 2 cases and of a small right coronary artery feeding only the right ventricle in one case. In the absence of electrocardiographic signs in the inferior territory, this ST elevation is suggestive of an anterior infarction in constitution, but the characteristic "dome-like" shape of the elevation, its decrease from V2 or V3 to V4 or V5 and the progressive regression of repolarization disorders without occurrence of Q wave suggest a diagnosis of right ventricular infarction. This diagnosis can rapidly be confirmed by a normal left ventricular function at echocardiography.