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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A unique case of congenital heart disease and complete heart block diagnosed by fetal electrocardiogram (ECG) and phonocardiogram recorded initially at 32 weeks gestation is presented. The slow, regular fetal heart rate of approximately 50 beats/min with bizarre QRS and a diamond-shaped murmur beginning with the fetal QRS complex made a diagnosis of complete heart block (CHB) and associated congenital heart disease highly probable. Direct fetal electrocardiograms (FECG) recorded during labor and vaginal delivery at term confirmed the diagnosis of completel atrioventricular block. Cardiac catheterization at 1 day of age showed multiple congenital heart anomalies. The infant developed signs of congestive heart failure and transvenous pacemaker was successfully placed; however, he died at 9 days of age of sepsis and renal failure.
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PMID:A new prenatal cardiac diagnostic device for congenital heart disease. 90 15

A 17-year-old woman with mitral and tricuspid valve prolapse and myxomatous degeneration presented puerperal infection by Staphylococcus aureus with clinical picture of sepsis and multiple septic embolism (right eye, left thumb, spleen, and left calf). She underwent total hysterectomy on the 10th day postdelivery and right eye enucleation on the 16th. Temporary total AV block occurred on the 14th day with temporary external pacing during the next couple of days. Acute endocarditis with acute mitral regurgitation was diagnosed on the 13th day, demanding immediate valve replacement. On the 46th day she developed moderate tricuspid valve regurgitation due to another episode of endocarditis. Final clinical discharge took place on the 62nd day after antibiotic therapy completion.
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PMID:[Staphylococcus aureus endocarditis in a puerperal woman with mitral and tricuspid valve prolapse]. 209 20

Cardiac illness in myotonic muscular dystrophy (MyD) is infrequent, but subclinical cardiac involvement in MyD is very common (found in 42 of 46 subjects) and may be responsible for sudden death. In this series, we found ECG abnormalities in 72%, left ventricular dysfunction in 70%, mitral valve prolapse in 37%, and sudden death in 4%. Four deaths during the study period were due to acute left ventricular failure, one to sepsis and respiratory insufficiency, and one was unexplained. We did not find ominous bradyarrhythmias or atrioventricular block, evidence of congestive heart failure, noninvasive evidence of coronary artery disease, or any correlation of type or amount of cardiac involvement with any clinical parameter such as age, sex, or severity of systemic dystrophy. We feel tachyarrhythmias may play as important a role in sudden death of myotonic muscular dystrophy subjects as bradyarrhythmias, and coronary artery disease in addition to cardiac dystrophy may produce arrhythmias and myocardial dysfunction in myotonic muscular dystrophy. In addition, some subjects have an unusual form of resting left ventricular dysfunction which improves with exercise. The most important problem in the clinical management of myotonic muscular dystrophy subjects is sudden death, and the solution does not appear to be empiric ventricular pacing. Our recommendations for prophylaxis of sudden death in myotonic muscular dystrophy are noninvasive investigation of coronary artery disease in subjects with significant risk factors, with angiography and surgery if indicated: detailed evaluation of syncopal and presyncopal events, including electrophysiologic testing, with pacemaker or antiarrhythmic drug therapy if indicated; and consideration of ventricular pacing of asymptomatic subjects if severe bradycardia or marked intraventricular conduction delay develops during follow-up, serial 12-lead ECGs. The documentation of tachyarrhythmias during sudden death and syncopal episodes in myotonic muscular dystrophy subjects makes ventricular pacing alone an uncertain modality for prevention of sudden death in subjects with only mildly lengthened PR or QRS intervals, and suggests a combination of pacemaker and antiarrhythmic drug therapy for the myotonic muscular dystrophy subject with syncope of no apparent cause.
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PMID:Cardiac involvement in myotonic muscular dystrophy. 405 3

As precursors of permanent pacemakers, Lidwill (1929) and Hyman (1932) introduced temporary pacemakers for resuscitation. Callaghan (1950) intravenously paced the sinus nodal region for bradycardia in hypothermic dogs. Zoll (1952) used external electrodes to treat Adams-Stokes attacks, and Lillehei (1957) fixed stainless steel electrodes to the myocardium, successfully treating iatrogenic total atrioventricular block with a percutaneous pacemaker. Since 1951, by experimental and clinical use of ventricular fibrillation to obtain a functional cardiac standstill during open heart surgery, we used all known methods of stimulation to treat asystole or bradycardia after defibrillation. Since 1957, percutaneous stimulation by Adam-Stokes attacks has been performed. The most serious complication is infections along the electrodes causing death from sepsis. The solution of the problem was the implantation of the pacemaker and its energy supply. Percutaneous leads were used to study the different parameters for electric stimulation and to find the lowest frequency (to spare energy) with the best variation of cardiac output. In October 1958 in Stockholm a fixed rate pacemaker was implanted by thoracotomy. At present, the patient is living with his 23rd pacemaker. Four additional patients had pacemaker implantations until 1960. In 1961, Chardack and Greatbach successfully implanted pacemakers with mercury batteries. Johanson and Lagergren connected the pacemaker to an intravenous electrode to avoid thoracotomy. The enormous development in the electronic field made more elaborate pacemakers possible, and eliminated the risk of the fixed rate (interference, repetitive firing, and ventricular fibrillation).
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PMID:Cardiac pacing in retrospect. 634 75

An international registry was formed to collate data for patients undergoing attempted catheter ablation of the atrioventricular (AV) junction and insertion of a permanent pacemaker. Over the past 2 years, data was submitted for 127 patients who were followed for a mean of 9.9 +/- 8.2 months. The most common arrhythmia treated was chronic or paroxysmal atrial fibrillation or flutter (78 patients, 61%); the remainder had supraventricular tachycardia due to AV node reentry, ectopic atrial tachycardia, or incorporated an accessory pathway. A single shock of 150 to 400 J was effective in producing chronic third-degree AV block in 45 patients while two or more shocks were used in an additional 45 patients. There was no significant difference in the total cumulative energy used in successful and unsuccessful procedures. Immediate complications related to the shock included ventricular fibrillation (one patient), pericardial tamponade (one patient), and transient hypotension (one patient). No chronic sequelae occurred as a result of these complications. Late complications (1 day to 1 month) included ventricular tachycardia (three patients), sepsis involving the pacemaker pocket (two patients), staphylococcal sepsis from temporary pacing catheter (one patient), thrombophlebitis (one patient), thrombosis of the left subclavian vein (one patient), and hemothorax (one patient). Follow-up evaluation revealed chronic third degree AV block in 90 (71%) and AV conduction resumed but no drugs were required for arrhythmia control in eight (6.5%) and arrhythmia control was achieved with previously ineffective drugs in 16 (13%). Thirteen patients (10%) had no improvement and five of these patients underwent cardiac electrosurgery for direct His bundle ablation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Catheter ablation of the atrioventricular junction: a report of the percutaneous mapping and ablation registry. 649 41

From August 1974 through April 1981, 23 patients, ages 5 months to 40 years (median 11 years) with corrected transposition of the great arteries (C-TGA), underwent repair of associated intracardiac defects: 20 for ventricular septal defect (VSD), 19 for pulmonary outflow tract obstruction, and five for anatomic tricuspid valve regurgitation. Segmental anatomy was [S,L,L] in 18 or [I,D,D] in 5. Pulmonary outflow tract obstruction was resected in 10 and bypassed with a left ventricle-to-main pulmonary artery conduit in nine patients. Hospital mortality was 9% (two of 23). One patient died from arrhythmia and one from sepsis and arrhythmia. The late mortality rate was 14% (three patients). Two patients died from severe pulmonary vascular obstructive disease (5 months and 2 years postoperatively) and one from arrhythmia (2 months postoperatively). Fourteen have undergone cardiac catheterization 3 days to 4 years (mean 12 months) postoperatively. Three had a small residual VDS (Qp/Qs less than 1.5). Five had residual pulmonary outflow tract obstruction (peak systolic ejection gradient 30-130 mm Hg) after resection or pulmonary valvotomy. One patient had reresection and four had placement of a secondary left ventricular-pulmonary artery conduit. Anatomic tricuspid valve regurgitation became severe in three patients after VSD closure, two of whom required valve replacement; the other died of coexisting pulmonary vascular obstructive disease. Five with [S,L,L] segmental anatomy had complete atrioventricular block preoperatively and six developed complete atrioventricular block at surgery. Eleven of 18 patients with [S,L,L] anatomy had atrioventricular spontaneous or iatrogenic complete block; none of the five patients with [I,D,D] anatomy had atrioventricular block. Pulmonary outflow tract obstruction in [S,L,L] segmental anatomy required conduit interposition in 12 of 14 of our patients to significantly decompress the ventricle. Postoperative development or exacerbation of anatomic tricuspid valve regurgitation occurs in TGA [S,L,L] and may be causally related to surgical complete atrioventricular block.
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PMID:Corrected transposition and repair of associated intracardiac defects. 708 42

In 1993, infectious endocarditis (IE) remains a common and serious condition. Surgery has become an essential feature of treatment in many cases. The choice and optimal timing depend on many factors: the tolerance of the underlying cardiac disease is an important feature, surgery being indicated not only in cases of necessity (refractory cardiac failure) but also as treatment of choice in cases of episodic decompensation even if temporary when related to valvular dysfunction. In these conditions, if the lesion is severe aortic incompetence, surgery can be programmed in two or three weeks after initiating antibiotic therapy; the bacteriological indications are less common: fungal endocarditis, prosthetic valve endocarditis due to gram-negative bacilli or staphylococcus aureus endocarditis, or IE on native valves with persistent signs of sepsis after one week of antibiotic therapy; the occurrence of some complications may require urgent surgery: high degree atrioventricular block, septal perforation, ring or perivalvular abscess detected at echocardiography, single or multiple systemic embolism with persistence of large, mobile vegetations at echocardiography. Conversely, tricuspid valve endocarditis usually respond well to medical treatment alone: surgery (valvuloplasty with excision of vegetations, valvulectomy or, preferably, bioprosthetic valve replacement) is sometimes indicated in septic states related to certain pathogenic organisms. The operative indications in 1993 have become more extensive and earlier: analysis of surgical results shows that operative mortality depends mainly on the haemodynamic status at the time of operation, but also on the severity of the anatomical lesions, the nature of surgery, the type of endocarditis, native or prosthetic valve, and the causal organism.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Surgery for bacterial endocarditis. When?]. 802 92

A 63-year-old woman admitted with 2:1 infranodal atrioventricular block subsequently developed ventricular dysfunction incident to septic syndrome. Concomitant changes included an abnormally prolonged QTc interval (600 ms) and the occurrence of torsade de pointes. Restoration of a normal QTc interval and cessation of torsade de pointes was coincident with return of normal ventricular function and remission of sepsis. This report supports the view that sepsis-induced cardiomyopathy is another cause of the long QT syndrome.
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PMID:Septic cardiomyopathy as a cause of long QT syndrome. 855 Nov 76

To examine the surgical indications and the results of the maze procedure, we reviewed 30 cases who underwent the maze procedure concomitantly with other open heart surgery from October 1995 to October 1997.: the average age was 60.9 years (37 to 75 years) and mean follow up period was 12.3 months (1 to 25 months). The modified maze procedure described by Kosakai and associates was applied in all patients. Twenty one patients (72.4%) regained atrial rhythm and eight patients (27.6%) sustained atrial fibrillation in the follow up periods. The left atrial diameter measured by echocardiography and cardiothoracic ratio were significantly larger in the latter group of patients, compared with those who recovered normal sinus rhythm (63.8 +/- 19.5 versus 51.2 +/- 7.8 mm and 67.7 +/- 8.1 versus 59.2 +/- 5.4%). In order to perform the combined maze procedure, cardiac arrest time and cardiopulmonary bypass time were extended for 56.9 minutes and 65.9 minutes, respectively, compared with the cases without a maze procedure. Four patients (brady atrial fibrillation 2, brady junctional rhythm 1, and complete AV block 1) required permanent pacemaker implantation. There was no operative death, but one patient who underwent the maze procedure and AVR + MAP + TAP died after 4 months due to pulmonary infection, sepsis and multiple organ dysfunction. This patient had shown low output syndrome for 3 days postoperatively. Having considered the data that the preoperative ejection fraction was 51%, cardiopulmonary bypass and cardiac arrest time were 200 min and 165 min respectively, occurrence of low cardiac output had been influenced by prolonged aortic cross-clamp. No late deaths have been observed in follow up period. In conclusion, maze procedure should not be performed in patients who have enlarged left atrium or complex cases requiring relatively longer operative time.
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PMID:[Evaluation of the results of the combined maze procedure for chronic atrial fibrillation with organic heart disease]. 1031 26

Patients with infective endocarditis usually developed persistent fever and heart failure, especially when the valve structures are invaded and destroyed. Persistent bacteremia often leads to severe sepsis or overwhelming septic shock. Septic emboli from the vegetation will possibly result in systemic thromboembolism with multiple organ infarction. Patients with infective endocarditis have been reported to present with either ruptured sinus of Valsalva or complete atrioventricular block. However, both of these serious complications occurring in a single patient is rare. In this case report, we present a 54-year-old man with a previous history of alcoholic cirrhosis and chronic renal failure who suffered from a fulminant course of infective endocarditis. Simultaneously, ruptured sinus of Valsalva and complete atrioventricular block further complicated the preexisting septic shock and multiple organ failure.
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PMID:Ruptured sinus of valsalva and complete atrioventricular block complicating fulminant course of infective endocarditis: a case report and literature review. 1691 22


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