Very low calorie diets and pre-fasting prolonged QT interval: a hidden potential danger

The asssociation of torsade de pointes and a prolonged electrocardiographic QT interval is well described. A prolonged QT interval may be congenital or acquired in several ways - by the use of anti-arrhythmic agents exemplified, by the presence of hypocalcaemia or hypokaemia, by the use of psychotropic drugs, and by the presence of intrinsic cardiac disease or bradycardias. Possible less well appreciated is the potiental for drastic weight loss to prolong the QT interval, as the present case report illustrates. A young woman weighing 244 pounds lost 24 pounds in two weeks with a consequent prolongation of QTc interval from pre-diet value of 0.57 seconds to 0.72 seconds at administration, when severly symptomatic paroxysms of torsade de pointes were recorded. Successful therapy with lignocaine and prompt re-feeding supressed the arrhythmia and, three days later, the QTc was reduced to almost its pre-diet state. A (UK) DHSS report offers guidelines in the use of very low caloric diets. This case suggests that a pre-diet electrocardiogram should be carefully assessed for QT prolongation before initiation of dieting to achieve serious weight loss (AU)

Modification of the cardiovascular responses to general anaesthesia by transdermal nitroglycerine - abstract

Low dose, transdermal nitroglycerine (TD-NTG) in a "nitropatch" formulation was used in an attempt to ameliorate the hypertensive, tachycardiac response to tracheal intubation. Observations were also made to elucidate whether TD-NTG 5 mg has any effect on the subsequent period of general anaesthesia and recovery. TD-NTG 5 mg patches were applied to ten young, healthy patients with ten similar patients as controls. Premedication, induction and the first four minutes of anaesthesia were standardized. Systolic (SBP), diastolic (DBP) and mean (MAP) arterial pressures along with heart rate (HR) were measured at constant intervals. Rate-pressure product (RPP), as an indicator of myocardial oxygen consumption, was derived for each set of measurements. There was a short-lived, significant (p<0.05) rise in all variables in both groups, during intubation. This rise was significantly lower for all variables (except HR) between the two groups. The increase in HR was similar between the groups. There were no significant differences in the pre-induction or recovery-room measurements between the groups. No gross differences were noted during the course of anaesthesia after intubation. The only side-effect noted was slight headache in TD-NTG patients. TD-NTG patches are a useful addition to the anaesthetic armoury of drugs to control blood pressure during intubation. Their removal before induction from patients using them for the control of angina must be carefully considered in the light of the present study's findings of no adverse effects during general anaesthesia (AU)

Chest pain: esophageal, cardiac, or both?

The esophagus may be the origin of chest pain clinically indistinguishable from that of ischemic heart disease. In some patients the esophageal origin of the pain may only be recognized by pharmacological provocation during manometry. We describe nine patients with chest pain which could be explained by disorders of esophageal motility-diffuse spasm in four, high pressure lower esophageal sphincter in three, and "nutcracker esophagus" in two. Methacholine provoked the pain and manometric abnormalities in five patients who had normal baseline tracings. However, seven patients given methacholine developed ischemic changes on the electrocardiogram. In one patient these were typical of Prinzmetal's variant angina. The mannometric and electrocardiographic abnormalities were reversed by intravenous atropine. Ischemic heart disease and esophageal motor disorders may occur concomitantly and pose a dilemma in diagnosis and management. (AU)