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years.
Left bundle branch block
Incomplete left bundle branch block is an ECG diagnosis which applies when the standard criteria for left
bundle branch block are satisfied (absent q wave in SI, aVL, V5 and V6; absent r’ in V1, with or without
secondary T wave changes) but the QRS complex width is <120ms. See Appendix 1b: 2. The distinction
is arbitrary. If long-standing and the heart is structurally and functionally normal, there appears to be little
or no increased risk, and such individuals need not be restricted.
In the event of new presentation, the structural integrity of the heart needs to be established with
echocardiography. The possibility of coronary artery disease needs to be considered and excluded with
pharmacological stress thallium MPI or coronary angiography as an exercise ECG is likely to be
abnormal due to secondary repolarisation change.
Complete left bundle branch block has had a malign reputation, partly on account of its association with
coronary artery disease in older subjects in whom the incidence may be as high as 25 to 50 per cent. It is
one-tenth as common as right bundle branch block in the general population. Newly acquired left bundle
branch block in one study observed a risk ratio for sudden cardiac death of 10:1 (i.e. 10 times greater than
expected) > age 45 years, although below that age the risk ratio was 1.3:1. Notwithstanding, stable
complete left bundle branch block appears to carry little excess risk of cardiovascular event in the
otherwise normal heart and may be consistent with multi-crew operation. See Appendix 1b: 17 for an
example and morphological description. Coronary angiography or pharmacological stress myocardial
perfusion imaging (MPI) is needed to exclude the possibility of coronary artery disease.
Applicants with the first presentation of left bundle branch block may be considered for a restricted
Class 1 (OML) Medical Assessment provided that:
• left ventricular function is normal, eg the ejection fraction is > 50 per cent as measured by
echocardiography (Simpson’s rule), multiple-gated acquisition (MUGA) study, or contrast
ventriculography
• exercise ECG to stage IV of the Bruce treadmill protocol can be achieved without evidence of
myocardial ischaemia, significant rhythm disturbance or symptoms
• pharmacological stress thallium MPI, or equivalent, shows no evidence of a reversible defect.
A small fixed defect is permissible, provided the ejection fraction is within the normal range
• coronary angiography, if carried out, demonstrates <50 per cent stenosis in any major untreated
vessel or in any venous/arterial graft remote from any infarction; <30 per cent if the proximal the
left anterior descending or left main-stem vessels are involved
• Holter monitoring, if indicated, shows no significant rhythm disturbance
• Annual follow up is carried out by a cardiologist acceptable to the Licensing Authority.
The Hemiblocks
ICAO Preliminary Unedited Version — October 2008 III-1-29
Left anterosuperior and left inferoposterior fascicular (hemi)blocks in the absence of other abnormality
appear to carry little or no excess risk of cardiovascular event in subjects of pilot age. The prevalence of
the former increases from 0.5 per cent at age 30 years to five per cent at age 60 years and in a few will
reflect coronary artery disease or progressive fibrosis of the conducting fascicles (Lenègre’s disease1). See
Appendix 1b: 14.
At first presentation > age 40 years, and if present at the initial issue of a licence, cardiological review
with exercise ECG and echocardiography is justified. If there is doubt, the possiblity of coronary artery
disease needs to be excluded with pharmacological stress thallium MPI or equivalent, particularly in the
case of acquired left anterior and posterior hemi-block. The emergence of a change in axis on routine
scrutiny justifies such review.
ION CHANNELOPATHIES
The ion channelopathies form a rare group of inherited disorders of the sodium and potassium channels
that regulate cardiac depolarisation. Over 250 mutations involving six different genes have been
identified. They are transmitted as autosomal dominants with incomplete penetrance and expression. They
are associated with ventricular tachycardia — torsades de pointes2 and sudden cardiac death —
commonly in the first two or three decades of life.
Brugada syndrome3 is transmitted as an autosomal dominant gene with incomplete penetrance. It appears
to be linked to the SCN5A gene which encodes the sodium channel. Its prevalence has been reported as
between five and 66 per cent per 100 000 but it is more common in the Far East and in Japan where the
　
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