Two experiments examined the relationship between Type A behavior and cardiovascular and plasma catecholamine responses to experimental competition and harassment. Experiment I showed that, in 44 male adults, the presence of a hostile opponent caused no significant differences in the responses of Type B's. In A's, by contrast, hostility elicited greater increases in systolic blood pressure, heart rate and plasma epinephrine during competition. Behavior pattern A appears selectively predisposed to enhanced reaction to hostile interactions, but competition alone does not distinguish between individuals with A and B behavior patterns. Experiment II, with 20 cases, was carried out to determine whether or not the absence of A‐B differences in the presence of a nonhostile competitor could be explained by Type B's reactivity to the challenge of competition alone. The results were consistent with this interpretation. A's showed greater blood pressure and plasma epinephrine evaluations than B's when both types were confronted by the challenge of task performance. Consideration was given to the role of sympathetic activation in mediating the tendency of Type A individuals to develop coronary heart disease.

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Cardiovascular, plasma catecholamine, and behavioral effects of control over aversive events were studied in 87 Type A and B male adults. Subjects performed a choice reaction time (RT) task during which they received loud noise bursts and/or electric shocks on designated trials. About half of the cases were told they could avoid noise and shock by attaining a predetermined criterion of RT speed (Contingency). The remaining half were instructed that noxious stimulation would be delivered randomly, irrespective of their performance (No Contingency). Half of the cases in each treatment were exposed to high frequency of aversive stimulation (High FAS), whereas the remaining half received low frequency of such stimulation (Low FAS). Within Contingency, High and Low FAS were designed to signify failure and success, respectively. Aversive stimulation in No Contingency was gratuitous and, therefore, did not convey information about performance. Relative to No Contingency, the Contingency treatment induced greater increases in RT speed, systolic and diastolic blood pressure, and plasma epinephrine. Differential FAS did not potentiate these differences. It also was found that the Type A subjects had higher systolic blood pressure and heart rate responses than Type B's. The prediction that Contingency (particularly with High FAS) would elicit greater physiologic and behavioral hyperresponsiveness in A's than B's received some support in the data for RT speed and plasma NE. Findings were discussed in terms of sympathetic activation of hemodynamic changes under conditions of active coping. Consideration was given to the role of the sympathetic nervous system and Type A behavior in cardiovascular disease.

Introduction In South Africa, an estimated 4.6 million people were accessing antiretroviral therapy (ART) in 2018. As universal Test and Treat is implemented, these numbers will continue to increase. Given the need for lifelong care for millions of individuals, differentiated service delivery models for ART services such as adherence clubs (ACs) for stable patients are required. In this study, we describe long‐term virologic outcomes of patients who have ever entered ACs in Khayelitsha, Cape Town. Methods We included adult patients enrolled in ACs in Khayelitsha between January 2011 and December 2016 with a recorded viral load (VL) before enrolment. Risk factors for an elevated VL (VL >1000 copies/mL) and confirmed virologic failure (two consecutive VLs >1000 copies/mL one year apart) were estimated using Cox proportional hazards models. VL completeness over time was assessed. Results Overall, 8058 patients were included in the analysis, contributing 16,047 person‐years of follow‐up from AC entry (median follow‐up time 1.7 years, interquartile range [IQR]:0.9 to 2.9). At AC entry, 74% were female, 46% were aged between 35 and 44 years, and the median duration on ART was 4.8 years (IQR: 3.0 to 7.2). Among patients virologically suppressed at AC entry (n = 8058), 7136 (89%) had a subsequent VL test, of which 441 (6%) experienced an elevated VL (median time from AC entry 363 days, IQR: 170 to 728). Older age (adjusted hazard ratio [aHR] 0.64, 95% confidence interval [CI] 0.46 to 0.88), more recent year of AC entry (aHR 0.76, 95% CI 0.68 to 0.84) and higher CD4 count (aHR 0.67, 95% CI 0.54 to 0.84) were protective against experiencing an elevated VL. Among patients with an elevated VL, 52% (150/291) with a repeat VL test subsequently experienced confirmed virologic failure in a median time of 112 days (IQR: 56 to 168). Frequency of VL testing was constant over time (82 to 85%), with over 90% of patients remaining virologically suppressed. Conclusions This study demonstrates low prevalence of elevated VLs and confirmed virologic failure among patients who entered ACs. Although ACs were expanded rapidly, most patients were well monitored and remained stable, supporting the continued rollout of this model.