No abstract

Rehabilitation after acute myocardial infarction (AMI) consists of education, exercise, and an encouragement to return to work (RTW). This study attempts to (1) determine whether the time interval between AMI and the visit at occupational medicine (OM) clinics predicts resumption of full employment, and (2) estimate the incidence of work-related recurrent AMI after RTW. We followed 216 consecutive AMI patients at a single OM clinic. The independent variables were clinical and personal data, physical workload and time between AMI, and first visit to the OM clinic. The outcome variables were full employment 24 months after the acute event and recurrent AMI during this period. Of all patients, 168 attempted RTW. Of these, 18 stopped working subsequently. Of the remaining 150 patients, 54 returned to part-time work and 96 were employed full-time after 2 years. Logistic regression indicated that a failure to resume full employment was independently associated with diabetes, older age, Q wave AMI, angina before AMI, heavy work, and a late visit to the OM clinic. For each month's delay in referral to the OM clinic, there was a 30% decrease in the chance for full employment 24 months after AMI. Six (4%) of the 150 patients who resumed employment sustained a recurrent AMI, two of them while at work. A delayed referral to the OM clinic was associated with work disability after AMI. Late referrals to OM clinics should receive a more intensive and sustained rehabilitation than early referrals. Whether an earlier referral to OM clinics will result in increased RTW rates is unknown. Patients who attempted to resume employment had a 1.2% risk of a recurrent ischemic event at their workplace.

Analyses of regional left ventricular systolic wall motion or thickening overestimate infarct size. We used quantitative two-dimensional echocardiographic analysis of systolic thickening and contrast two-dimensional echocardiography to evaluate causes for that overestimation. The following possibilities were considered: (1) "tethering," defined as dysfunction of contrast-enhancing myocardium adjacent to ischemic or contrast-negative regions, and (2) the role of standard center of mass analysis algorithms, which may overestimate wall motion abnormalities because of the axis shift produced by simultaneous systolic expansion of the ischemic segment and systolic contraction of the nonischemic segment. In the short-axis view in 12 animals, the echo contrast defect (ECD) occupied 32 + 7% of the left ventricular circumference. Extent of dysfunction by the center of mass analysis was 39 + 5% of the left ventricular circumference and correlation with ECD size was .68 (SEE = 5.2%). Thus 8 -+-6% of the circumference of the left ventricle was assessed to be dysfunctional yet enhanced with contrast. Tethering accounted for only half of this (4 + 4% of left ventricular circumference) and involved less than 1 cm on either side of the ECD. The remaining overestimation by the center of mass analysis correlated significantly (r = .89, p < .01) with the amount of systolic expansion of the ECD. This expansion of the ECD (increase in angle subtended by the ECD of 11 ± 8%) was produced by the systolic shift in the center of mass toward the dysfunctional segment from contraction of the opposite, nonischemic segment, since true systolic lengthening of the ischemic (contrast-negative) segment was minimal (increase of only 3 + 5%; p < .01 vs increase in angle subtended by ECD). When systolic function was analyzed independent of a center of mass with the ECD as an internal reference, the correlation between extent of dysfunction and ECD size improved to .84 (SEE = 3.8%). In conclusion, two-dimensional echocardiography has exaggerated the importance of tethering because of flaws in standard analysis algorithms. Tethering does lead to an unavoidable overestimation of infarct size, but the amount of myocardium involved is small and relatively predictable. The remainder of the overestimation of infarct size by two-dimensional echocardiography is critically dependent on systolic function of the opposite, nonischemic wall. Since this is variable, it accounts in large part for the suboptimal correlation between infarct size and extent of dysfunction by standard two-dimensional echocardiographic analyses. Circulation 73, No. 6, 1360-1368, 1986 TWO-DIMENSIONAL echocardiography could in theory be an ideal technique for studying the effects of interventions to limit infarct size. However, two-dimensional echocardiographic analyses of either regional left ventricular systolic wall motion or thickening consistently overestimate infarct size. '-13

In South Africa (SA), surveillance for respiratory diseases, diarrhoea and meningitis has been used to define the epidemiology, aetiology and seasonality of these syndromes. [1-5] Healthcare utilisation surveys have been used to provide meaningful interpretation of surveillance data. [6-8] These surveys provide estimates of the proportion of illness episodes not captured by health facility-based surveillance, which is most commonly used to estimate the burden of disease. While facility-based surveillance provides more accurate diagnoses, it may underestimate the burden of disease by omitting individuals who do not seek care at formal healthcare facilities. In addition, there are several barriers to care seeking that include shortages of staff, equipment or drugs as well as distance from healthcare facilities and high travel costs [9-11] and may lead to a proportion of people not seeking healthcare through clinics or hospitals. Healthcare utilisation This open-access article is distributed under Creative Commons licence CC-BY-NC 4.0.

We studied the effect of transcendental meditation (TM) on breathing using 16 experienced meditators and 16 control subjects. In controls, there was no significant difference in minute ventilation (VE), respiratory pattern, or hypercapnic response, whether breathing with eyes open-awake (CA), or with eyes closed-relaxing (CR). In meditators, VE decreased significantly during quiet breathing from 14.0 +/- 0.7 1/min with eyes open-awake (MA) to 12.4 +/- 0.6 1/min during meditation (MM) (P less than 0.02). The change in VE during meditation was due to a decrease in tidal volume (VT) resulting from a shortened inspiratory time (TI). Meditation was associated with a decreased response to progressive hypercapnia from 3.7 +/- 0.4 to 2.5 +/- 0.21 X min-1 X Torr-1 during MA and MM trials, respectively (P less than 0.01). During meditation VT was smaller at a given alveolar PCO2 than during MA studies because of a decrease in mean inspiratory flow rate (VT/TI). These observations suggest that an alteration in wakefulness, more subtle than sleep or the unconscious state, can significantly affect the chemical and neural regulation of breathing.