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3 results

  • Unexpected and atypical clinical presentation of myocardial infarction in infants and children: complex pathogenesis of progressive and lethal disease

  • Amr Matoq, Gina Patel, Takeshi Tsuda
  • Journal:
    Cardiology in the Young , First View
    Published online by Cambridge University Press:
    08 October 2024, pp. 1-8
    • Article
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  • Background:

    Myocardial infarction is rare in children but frequently occurs unexpectedly with atypical presentation. It can cause a progressive lethal course unless prompt treatment is initiated.

    Methods:

    Paediatric cases of myocardial infarction diagnosed by the presence of ischaemic myocardial insults and symptomatic ventricular dysfunction were reviewed retrospectively.

    Results:

    Eighteen patients (5 days to 14 years of age; median 3 months) with myocardial infarction were studied. The aetiology was variable, including congenital coronary anomalies: anomalous left coronary artery from pulmonary artery (five patients), pulmonary atresia with intact ventricular septum with right ventricle-dependent coronary circulation (four), anomalous aortic origin of left coronary artery (three), and Williams syndrome with supravalvar aortic stenosis (one). Two acquired coronary anomalies occurred in one patient with undiagnosed Kawasaki disease with complete thrombotic obstruction of the left coronary artery and another with post-transplant cardiac allograft microangiopathy. Three patients developed thromboembolic coronary artery incidents in normal coronary anatomy. Fourteen patients were less than 1 year of age (78%). Electrocardiographic abnormalities were noted in all patients. Four patients required extracorporeal membrane oxygenation support for severe ventricular dysfunction, none of whom survived. Five patients underwent heart transplant. Five patients died during the same hospitalisation, and one patient died after discharge (overall mortality 33%). Transplant-free survival was 39%.

    Conclusion:

    Most myocardial infarction occurred in infants who presented with abrupt onset of non-specific clinical manifestations with progressively deteriorating haemodynamic status resulting in poor transplant-free survival rate. Early diagnosis and treatment are essential to prevent catastrophic outcomes.

  • Chapter 41 - Cerebellar infarcts

  • from Section 2 - Vascular topographic syndromes
  • Edited by Louis R. Caplan, Jan van Gijn
  • Book:
    Stroke Syndromes, 3ed
    Published online:
    05 August 2012
    Print publication:
    12 July 2012, pp 469-479

  • Summary

    Anatomically, each thalamus lies rostral to the brainstem, lateral to the third ventricle, and medial to the internal capsule. As most blood to the thalamus arrives from the tip of the basilar artery and the proximal portions of the posterior cerebral arteries (PCAs), thalamic lesions may be associated with simultaneous lesions in the midbrain or in the distal territory of the PCA. Microangiopathy is the cause of most lateral thalamic infarcts although embolic sources are occasionally found. Large thalamic hemorrhages involve more nuclei and tracts, with or without ventricular extension, resulting in overlapping clinical syndromes. Common features seen in patients with thalamic hemorrhages include rapid onset of symptoms, inconstant impairment of consciousness even in large size hematomas, and a relatively good prognosis as compared with that for hemorrhages in the pons and basal ganglia. Venous thrombosis of the deep cerebral venous system usually leads to bilateral thalamic edema.

  • Structural abnormalities do not explain the early functional abnormalities in the peripheral nerves of the streptozotocin diabetic rat

  • DAVID WALKER, ANNE CARRINGTON, SUSAN A. CANNAN, DIANE SAWICKI, JANET SREDY, ANDREW J. M. BOULTON, RAYAZ A. MALIK
  • Journal:
    The Journal of Anatomy / Volume 195 / Issue 3 / October 1999
    Published online by Cambridge University Press:
    01 October 1999, pp. 419-427
    Print publication:
    October 1999

  • The streptozotocin (STZ)-diabetic rat, the most commonly employed model of experimental diabetic neuropathy, is characterised by a reduction in nerve conduction velocity, pain threshold and blood flow. Whether or not structural abnormalities underlie these functional abnormalities is unclear. 10 adult male Sprague–Dawley STZ-diabetic rats (diabetes duration 27 d) and 10 age-matched (23 wk) control animals were studied. Motor nerve conduction velocity (m s−1) was significantly reduced in diabetic (41.31±0.8) compared with control (46.15±1.5) animals (P<0.001). The concentration of sciatic nerve glucose (P<0.001), fructose (P<0.001) and sorbitol (P<0.001) was elevated, and myoinositol (P<0.001) was reduced in diabetic compared with control animals. Detailed morphometric studies demonstrated no significant difference in fascicular area, myelinated fibre density, fibre and axon areas as well as unmyelinated fibre density and diameter. Endoneurial capillary density, basement membrane area and endothelial cell profile number did not differ between diabetic and control animals. However, luminal area (P<0.03) was increased and endothelial cell area (P<0.08) was decreased in the diabetic rats. We conclude there is no detectable structural basis for the reduction in nerve conduction velocity, pain threshold or blood flow, observed in the streptozotocin diabetic rat.