Improvement in exercise haemodynamics by isosorbide dinitrate in patients with severe congestive cardiac failure secondary to ischaemic heart disease.

Seven patients with severe chronic congestive cardiac failure secondary to ischaemic heart disease performed submaximal supine exercise before and after 5 mg sublingual isosorbide dinitrate at the time of cardiac catheterisation. Exercise before isosorbide dinitrate produced a poor response in left ventricular performance. After isosorbide dinitrate this response was significantly improved. Compared with the control exercise period, cardiac index increased from mean 2.6 to 3.1 1/min per m2 (P less than 0.0025), stroke volume index from mean 22 to 27 ml/m2 (P less than 0.0025), and left ventricular stroke work index from mean 21 to 30 g m/m2 (P less than 0.01). Mean left ventricular filling pressure fell from 37 to 26 mmHg (P less than 0.01). Although isosorbide dinitrate reduced left ventricular filling pressure at rest from mean 26 to 17 mmHg (P less than 0.005), there was no significant change in mean cardiac index or stroke volume index, while left ventricular stroke work index decreased from mean 29 to 22 g m/m2 (P less than 0.05). Isosorbide dinitrate effectively reduces left ventricular filling pressure in the resting patient with congestive cardiac failure but produces a more comprehensive improvement in left ventricular performance during exercise.     

Difficulties in the use of electrocardiographic criteria for the differential diagnosis of left bundle branch block pattern tachycardia in patients with a structurally normal heart.

In patients with left bundle branch block pattern tachycardia, electrocardiographic criteria, based on leads V1, V2 and V6, have been shown to be effective for the diagnosis of ventricular tachycardia in patients with a previous myocardial infarct. To test these criteria on a wider population, we studied 53 consecutive patients with left bundle branch block pattern tachycardia. Seventeen patients had supraventricular tachycardia and 36 had ventricular tachycardia, 18 with a previous myocardial infarction, two with cardiomyopathy, and 16 with a normal heart. The sensitivity for the diagnosis of ventricular tachycardia in patients with a previous myocardial infarct of the combined criteria was 100% but was only 50% for the other patients, which was not significantly different from the patients with supraventricular tachycardia (29%). Two other criteria, right axis shift in tachycardia and ventricular ectopics during sinus rhythm with the same morphology as the tachycardia, were only seen in patients with ventricular tachycardia, and combined with the other criteria allowed the correct identification of 35/36 patients with ventricular tachycardia. To conclude, the electrocardiographic criteria based on leads V1, V2 and V6 are not sensitive for the diagnosis of a ventricular origin of left bundle branch block pattern tachycardia in patients with a normal heart and additional criteria are required for the diagnosis in these patients.     

Implantable electrical devices in the management of tachyarrhythmias

Electrical therapy for tachyarrhythmias attempts to achieve one or more of three aims: a) prevention of tachycardia; (b) control of the hemodynamic effect of tachycardia; (c) termination of tachycardia. In practice, long term control of tachycardia in selected patients can be achieved with implantable devices which can automatically recognize and terminate tachycardias. Termination can be achieved with a number of pacing modalities. These pacing modalities are reviewed in this article and some guidelines to the choice of modality are given. Patients with supraventricular tachycardia are often more appropriately treated with drugs or surgery but some can be effectively treated with antitachycardia pacing. Some patients with ventricular tachycardia can be successfully treated with these devices but this group is at risk of tachycardia acceleration or degeneration in response to pacing. An implantable cardioverter-defibrillator should be used as a backup in these patients. Present generation devices now incorporate antitachycardia pacing, low energy cardioversion, and higher energy defibrillation in the same unit.     

Correlation between von Willebrand factor antigen,von Willebrand factor ristocetin cofactor activity and factor VIII activity in plasma

Background The laboratory diagnosis of von Willebrand Factor (VWF) deficiencies includes qualitative and quantitative measurements of VWF and clotting factor VIII (FVIII). Since the FVIII activity is frequently normal in patients with mild type 1 or 2 von Willebrand disease (VWD), there is controversy whether FVIII testing should accompany VWF Antigen (VWF:Ag) assay. Methods The aim of this study was to explore the correlation between VWF:Ag, VWF ristocetin cofactor activity (VWF:RCo) and FVIII in 213 consecutive patients undergoing screening for VWD. Results Forty-six patients were identified with VWF:Ag levels lower than the diagnostic threshold (54 IU/dl). A significant correlation was observed between VWF:Ag and VWF:RCo (r = 0.892; p < 0.001), VWF:Ag and FVIII (r = 0.834; p < 0.001), VWF:RCo and FVIII (r = 0.758; p < 0.001). Receiver operating characteristic curve analysis of the VWF:Ag assay revealed an area under the curve of 0.978 and 0.957 for detecting life-threatening values of FVIII (<30 IU/dl) and VWF:RCo (<40 IU/dl), respectively. The negative and positive predictive values at the VWF:Ag threshold value of 54 IU/dl were 100% and 33% for detecting life-threatening FVIII deficiencies, 94% and 80% for identifying abnormal values of VWF:RCo. Conclusions Due to the excellent correlation between VWF:Ag and FVIII and to the diagnostic efficiency of VWF:Ag for identifying abnormal FVIII levels in patients with VWF deficiency, routine measurement of FVIII may not be necessary in the initial screening of patients with suspected VWD. However, the limited negative predictive value of VWF:Ag for identifying type 2 VWD does not allow to eliminate VWF:RCo or VWF:FVIIIB assays from the diagnostic workout.     

Prevalence of folic Acid and vitamin B12 deficiencies in patients with thyroid disorders

Although macrocytosis might occur with frequency in patients with thyroid disorders, there is controversial information on the metabolic relationship between thyroid stimulating hormone (TSH), folic acid and B12 in the general population. We performed a retrospective analysis to retrieve results of serum folic acid, B12, and TSH performed on consecutive outpatients referred by general practitioners for routine blood testing over the last 2 years. A positive, significant trend towards increased values of folic acid, but not of B12, could be observed across the spectrum of TSH values suggestive for hypo- and hyperthyroidism. However, the prevalence of subjects with folic acid or B12 deficiency did not differ significantly among the subgroups of subjects. In multivariable linear regression analysis folic acid, but not B12, was associated with TSH levels. These results do not support the routine screening for either B12 or folic acid deficiency in subjects with subclinical disturbances of thyroid function, though we can not rule out that it might still be useful in patients with overt thyroid dysfunction.     

Electrophysiological characteristics of junctional pacemakers in congenital A-V block and following his bundle cryoablation

The characteristics of the escape mechanism following surgically induced permanent A-V block were investigated and compared with those seen in congenital complete heart block (CHB). Six patients had undergone elective cryothermal ablation of the His bundle for supraventricular arrhythmias unresponsive to pharmacological and pacemaker techniques (group A) and 12 patients had congenital CHB (group B). In the 12 patients in group B the site of block was localized by His bundle electrocardiography to be proximal to the point of recording of the His potential. In 3 patients in group A in whom intracardiac studies were performed it was impossible to record an His potential. There were no significant differences between the control escape rate, junctional recovery time (JRT), and corrected junctional recovery time (cJRT) of the two groups. In group A there were no significant changes in these parameters following the administration of atropine, whereas isoproterenol significantly increased the rate of the subsidiary pacemaker (p < 0.001) and shortened the JRT (p < 0.02) and cJRT (p < 0.02). In group B both atropine (A) and isoproterenol (I) significantly increased escape rate (A, p < 0.001; I, p < 0.001) and shortened JRT (A, p < 0.01; I, p < 0.001) and cJRT (A, p < 0.01; I, p < 0.001). It is concluded that the escape focus in patients with congenital CHB is situated in the A-V node. The escape rhythm following His bundle section is unpredictable and elective permanent pacemaker implantation is indicated.     

Effect of intravenous adenosine on human atrial and ventricular repolarisation.

OBJECTIVE: The aim was to assess the effects of therapeutic doses of intravenous adenosine on human atrial and ventricular repolarisation. METHODS: The effects of 6 mg and 12 mg bolus doses of adenosine on the atrial and ventricular monophasic action potentials were studied using the contact catheter technique in 19 patients undergoing routine diagnostic electrophysiology studies. The effect on atrial repolarisation was studied before and after beta blockade in a subgroup of patients. RESULTS: The duration of the monophasic action potential to 90% repolarisation (MAPD90) was measured in all cases. After 6 mg of adenosine the atrial MAPD90 shortened from 227(SD 29) ms to 188(25) ms (p < 0.005); after 12 mg it shortened from 221(31) ms to 168(32) ms (p < 0.001). The maximum shortening was unaltered by propranolol 0.15 mg.kg-1. The ventricular MAPD90 showed no significant change after 12 mg, at 240(32) ms v 234(33) ms. CONCLUSIONS: Therapeutic doses of adenosine shorten the atrial but not the ventricular monophasic action potential duration. The effect is dose dependent and not abolished by beta blockade.     

Adenocarcinoma of the ileoanal pouch anastomosis: an emerging complication?

BACKGROUND AND AIMS: Restorative proctocolectomy with ileoanal pouch anastomosis (IPAA) is currently the surgical treatment of choice for ulcerative colitis. Although dysplastic changes to the native ileal mucosa of the pouch occur in a subgroup of patients with severe chronic pouchitis, the development of cancer in the pouch itself is a very rare event. To date, only two cases of carcinoma of the IPAA have been reported, namely in patients operated on for colon cancer complicating ulcerative colitis and with a previous diagnosis of backwash ileitis. CASE REPORT: We report a patient with carcinoma in an ileoanal pouch who had been suffering from chronic atrophic pouchitis early after surgery. He had no previous history of colon cancer or backwash ileitis. The adenocarcinoma was detected 22 months after IPAA, and it was deeply infiltrating the adjacent structures (pT4N0M0, grade 2). Histology revealed the passage from chronic atrophic pouchitis to dysplastic epithelium and to cancer. CONCLUSION: Our case suggests that malignant transformation of the IPAA may occur as a pure complication of the severe chronic pouchitis, even in the absence of backwash ileitis or a previous history of colon cancer.