Tricuspid valvular disease is a common manifestation of the midgut carcinoid syndrome and advanced changes are associated with poor long-term survival. Active surgical and medical therapy of the tumour disease reduced the hormonal secretion and, combined with cardiological surveillance, made right ventricular heart failure a rare cause of death in these patients.
The aim of the present investigation was to discover whether disturbed left ventricular (LV) function limits renal replacement therapy in patients with juvenile onset diabetes mellitus. Seventeen patients given functioning kidney grafts were studied non-invasively (M-mode echocardiography, apexcardiography, phonocardiography) before renal transplant and an average of six, 13 and 44 months after transplant. The main pretransplant findings were pronounced LV hypertrophy with impaired diastolic LV function (prolonged relaxation time + signs of decreased LV distensibility) and a hyperdynamic circulation. Most of these abnormalities were significantly less severe after successful kidney transplantation. LV mass decreased by 37% 44 months after transplant (p less than 0.01) and LV diastolic and systolic volumes decreased with a subsequent increase in ejection fraction from 0.65 to 0.78 (p less than 0.01). The LV distensibility and filling pattern improved significantly while the prolonged relaxation time was unchanged. These findings imply that pretransplant disturbances in LV function are related more to factors such as hypertension, volume overload and uraemia than to diabetes per se because no pronounced improvement in the metabolic disorder resulting from diabetes can be expected, even after the most successful transplant. Disturbed LV function should not, therefore, exclude uraemic diabetics from renal replacement.
A 22-year-old man underwent electrophysiological evaluation for incessant wide QRS complex tachycardia with a pattern of right bundle-branch block and left axis deviation. The right and left ventricles were enlarged and hypokinetic consistent with dilated cardiomyopathy. Ventricular tachycardia was diagnosed by demonstrating capture and fusion beats, atrioventricular dissociation, and His potential activation that began after the onset of each QRS complex. Atrial extrastimuli and rapid atrial pacing failed to terminate the tachycardia and, although ventricular stimulation was successful, the tachycardia spontaneously restarted after one or two sinus beats. The tachycardia was unexpectedly abolished during catheter manipulation in the left ventricle and has not recurred during three-years of follow-up. The picture of a cardiomyopathy resolved. The ease with which the tachycardia was abolished by catheter manipulation implicate a therapeutic potential for catheter ablation of this type of tachycardia.
In a previous haemodynamic examination, 44 young men (18-22 years) with blood pressure elevation above the 98th percentile, mean arterial blood pressure (MAP) greater than or equal to 95 +/- 6 mm Hg, showed an increased cardiac index (dye-dilution) and an enhanced resistance at maximal vasodilation of the hand (venous occlusion plethysmography during hyperaemia). This latter finding suggested arteriolar wall hypertrophy. However, the subgroup with the highest cardiac index (greater than or equal to 3.86 1 min-1 x m2) (n = 18) displayed normal vascular resistance at maximal dilation in comparison with the normotensive control group (n = 29). Consequently, functional signs of arteriolar hypertrophy were restricted to individuals with normal or low cardiac index. At the re-investigation 5 years later, a significant reduction in blood pressure was observed in the normotensive control group (MAP: from 88 +/- 7 to 85 +/- 7 mm Hg, P less than 0.05). There was no change in individuals with initially elevated blood pressure. Furthermore, cardiac index fell significantly with time in this latter group. Thus, the blood pressure elevation in the hypertensive group, previously mainly dependent on high blood flow was, 5 years later, more related to an increased total peripheral resistance, (delta total peripheral resistance = 8%). However, no definite evidence indicating development of hypertrophy of the resistance vessels of the hand was observed during the follow-up period. Since the hyperkinetic subgroup did not display a concomitant fall in blood pressure with cardiac output, our results do not support the theory that the hyperkinetic form of borderline hypertension is a temporary phenomenon, explained by the inclusion of anxious individuals afraid of the experimental situation. Hyperkinetic hypertension may be the initial phase of sustained hypertension in a subgroup of the future hypertensive population.
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