Quantifying the impact of equity, diversity, and inclusion in electrophysiology: Training the first female electrophysiologists from Jamaica and Saint Lucia.

Background: Delivery of electrophysiology (EP) care in developing nations and underserviced populations faces many hurdles, including the lack of local expertise and knowledge creation. The West Indies has experienced a paucity of local EP expertise. The University of Toronto has undertaken a unique collaborative educational effort with the University of the West Indies. Objective: We describe the effects of equity, diversity, and inclusion (EDI) in EP training at Toronto General Hospital in Canada by quantifying the impact of training the first female electrophysiologists to practice in Jamaica and Saint Lucia. Methods: Data from the ministries of health in Jamaica and Saint Lucia were reviewed. The number of arrhythmia clinic patients seen, EP studies and ablations performed, pacemaker clinic patients seen, and implantable devices, permanent pacemakers (PPMs), and implantable cardioverter-defibrillators (ICDs) implanted were assessed. Results: One hundred one arrhythmia consults were seen by the new electrophysiologist in Jamaica after her return from training in 2020. She has since performed 19 EP studies/catheter ablations at a newly established ablation laboratory. Three cases of left ventricular (LV) dysfunction due to tachy-cardiomyopathy were treated successfully with catheter ablation with immense improvement in LV ejection fraction. Thirteen PPMs, 1 ICD, and 3 LV leads were implanted, after which no early complications were identified. In Saint Lucia, where there is no dedicated electrophysiology laboratory, 2 patients who required catheter ablation for tachycardia-mediated LV dysfunction were identified by the electrophysiologist since her return to the island in 2018. The patients were appropriately referred, resulting in restoration of normal LV function. Six PPMs also were implanted in Saint Lucia. Knowledge translation has been limited by the lack of accessibility to the required devices, catheters, and specialized equipment and accessories, mainly because of their costs. Conclusion: Training the first female electrophysiologists from Jamaica and Saint Lucia led to a quantifiable impact on EP care in both of these Caribbean countries. EDI strategies in EP training programs provide much needed benefits to developing nations, but more support is needed to allow new electrophysiologists to fully utilize their EP training to care for underserviced populations.

The incidence and management of life-threatening arrhythmias occurring during the course of acute myocardial infarction - abstract

During the last decade the early detection and successful treatment of life-treatening arrhythmias have resulted in a significant reduction in the mortality rate of patients with myocardial infarction. The purpose of this study was to determine the incidence of these dangerous arrhythmias and to explore the possibility of producing a similar reduction in mortality rate with our limited resources. Since the 1st July, 1971, all patients with clinical diagnosis of acute myocardial infarction have been admitted to a coronary bed in either the intensive care unit or one of our general medical wards. Each be is fully equipped with a cardioscope for the continual monitoring of the patient's electrocardiogram, a defibrillator/cardioverter and the necessary anti-arrhythmic drugs and resuscitative equipment. During the first 7 months of this project a total of 24 patients with unequivocal evidence of myocardial infarction were admitted to the study and their rhythm was continually monitored for period varying from at least 48 hours up to 21 days. Four patients died from cardiogenic shock and in addition 2 of these patients had bronchopneumonia. Nine of the 24 patients showed a significant rhythm change (40 percent) and of these, 5 patients (20 percent) had a life-threatening arrhythmia. These included (a) fast atrial fibrillation, (b) sinus bradycardia with Stokes-Adams attacks, (c) complete heart block with Strokes-Adams attack, (d) ventricular tachycardia and (e) ventricular fibrillation were treated with a combination of practolol and digoxin with cardioversion being reserved for resistant cases. Sinus bradycardia was treated with frequent doses of atropine (0.6 mgm. I.M. 2 to 6 hourly) and complete heart block was controlled by transvenous endocardial pacing. Lignocaine was used as the drug of choice for ventricular tachycardia and so far there have been no cases of ventricular tachycardia which have been resistant to this drug. Ventricular fibrillation was treated with immediate defibrillation starting at an energy level of 300 Watts Seconds. It is concluded that serious arrhythmias do occur in at least 20 percent of our patients with acute myocardial infarction and we have demonstrated that these can be successfully treated here (AU)

Studies on acid excretion in adults with sickle-cell anaemia

The acid excretion of patients with sickle-cell anaemia has been studied. There is a mild defect in urinary acidification and a decreased H+ excretion in response to ammonium chloride loading. The acidification defect was not corrected by oral administration of a phosphate solution. Infusion of sodium sulphate solution in subjects who were avidly reabsorbing sodium produced equal degrees of urine acidification in patients and controls. Studies on bicarbonate reabsorption were inconclusive. We conclude that patients with sickle-cell anaemia have a mild form of incomplete distal renal tubular acidosis (AU)

Peritoneal dialysis in severe leptospiral renal failure

Three cases of severe leptospiral renal failure have been described. They had all intrinsic renal damage and were treated satisfactory by peritoneal dialysis. Renal biopsies were done in 2 patients in the recovery phase of their illness and showed signs of severe tubular damage (AU)

Renal failure in human leptospirosis

The mortality rate in severe human leptospirosis may be as high as 30 percent and acute renal and hepatic failure are the most serious life threatening complications. The present report outlines the management of the last 3 patients admitted to the University Hospital with severe leptospirosis complicated by renal failure. They all had the biochemical indices of acute parenchymal renal damage and all 3 had to be dialysed. In one patient a total blood volume exchange transfusion had to be done. The records of 23 other patients with leptospirosis admitted to the University Hospital over the past 4 years have been reviewed. Of these 23 patients 5 died. In the survivors the mean blood urea on admission was 89mg/100ml and this had fallen to normal levels on discharge. A blood urea greater than 200 mg percent was seen in only 3 of the 18 survivors but in all 5 fatal cases. Early dialysis is recommended in the management of acute renal failure in leptospirosis (AU)

Acid-base balance in adults with sickle cell anaemia

This study of acid-base balance in adults with sickle cell anaemia was undertaken because of the reports of severe metabolic acidosis during "Painful Crisis". Metabolic acidosis has been incriminated as the cause of the "Painful Crisis" and it has been claimed that alkali treatment can prevent and even abort these painful episodes. It was therefore possible that a defect in urinary acidification could explain this tendency to develop acidosis with its serious consequences. The results of acid-base parameters during the steady state showed a mild respiratory alkalosis which is a non-specific finding in patients with severe anaemia. The response to oral NH4Cl loading revealed a slight but significant defect in urinary acidification (minimum pH in SCA 5.38 against 4.83 for controls). Titratable Acid excretion was reduced but the urinary NH4+ though reduced was normal when related to the urine pH. The glomerular filtration rate was normal. These findings are compatible with the syndrome of Incomplete Renal Tubular Acidosis. The administration of oral neutral phosphate resulted in a marked increase in titratable acid excretion but the defect in urinary acidification persisted. A maximal acidifying stimulus (Na2SO4 infusion) produced intense urinary acidification in both normal controls (minimum pH 4.55) and patients with SCA (minimum pH 4.59). Since the sulfate infusion is a known test of distal tubular acidification, a gradient type defect (Distal RTA) was ruledout. The threshold for bicarbonate excretion was reduced in 3 of 6 patients and it was therefore suggested that these patients have a form of Proximal Renal Tubular Acidosis due to defective bicarbonate reabsorption. There was no evidence of metabolic acidosis during "Painful Crisis". This would suppport our belief that Alkalis are of little use in the treatment or prevention of "Painful Crises", at least in our population (AU)

Acid-base status of adults with sickle-cell anaemia

Determinations of the acid-base status of 10 adult Jamaican patients with sickle-cell anaemia during "painful crisis" and after recovery showed no evidence of metabolic acidosis in the former, in contrast to reports from elsewhere. These results could explain the failure of alkalis to abort or alter the acute painful episodes of most patients with sickle-cell anaemia (AU)

Acid excretion in adults with sickle cell anaemia

Patients with sickle cell anaemia in painful crisis often have a severe metabolic acidosis. The purpose of this investigation was to determine if there is any abnormality of renal function, peculiar to patients with sickle cell anaemia which might affect their ability to excrete an acid load and hence provide an explanation for this tendency to develop acidosis. Adult patients with sickle cell anaemia - not in crisis - were given a standard load of ammonium chloride orally (0.1 gm./kgm. body weight). Urine was collected under paraffin oil every hour for a total of eight collections after the ammonium chloride was given. The pH, titratable acid and ammonia were determined on each hourly collection. The results have shown that these patients cannot excrete an acid load as efficiently as normal controls. The lowest urine pH obtained was 5.3 compared with 4.8 in the controls. Their excretion of titratable acid was markedly depressed, and the excretion of urinary ammonia, though normal for the pH obtained, was also low. As a result of this impairment of excretion of titratable acid and ammonia, excretion of total hydrogen iron (H+) was markedly reduced. The mechanisms of these defects and their relation to the other manifestations of sickle cell anaemia are being investigated (AU)

Defect in urinary acidification in adults with sickle-cell anaemia

Eight adult patients with sickle-cell anaemia have been shown to have a significant defect in urinary acidification. After a standard dose of ammononium chloride the lowest mean urine pH obtained was 5.42 compared with 4.85 for the controls. There was no accompanying systemic acidosis (AU)