Neuron SA - Vol 16 No 2 - Issue 51 - 2023

Introduction

Climate change and cardiovascular disease in Africa

Climate change has resulted in droughts, water scarcity, extreme weather events, severe fires, and declining biodiversity. These sudden changes in our environment are likely to have both direct and indirect effects on patients and increase the risk for cardiovascular disease. The main consequences of climate change affecting cardiovascular disease are extreme weather events, air pollution, water scarcity and healthcare pressures due to migration and urbanization. In this manuscript we briefly discuss some of the consequences of climate change and its adverse relationship to cardiovascular health, some of the putative mechanistic links with cardiovascular disease, the influence of healthcare industry in contributing to increased greenhouse gas emissions and mitigation strategies from a healthcare perspective to limit these emissions.

Greenhouse gases are at their highest levels in 2 million years. As a result, the earth is now 1.1 degrees Celsius warmer than it was in the late 1800s. The effects of these changes are becoming evident across the globe resulting in droughts, water scarcity, extreme weather events, severe fires, rising sea levels, and declining biodiversity. It is likely that land temperatures in Africa will rise faster than the global average, especially in more arid regions, with projections indicating that extensive areas of Africa will exceed 2°C by the last 2 decades of this century, relative to the late 20th century mean annual temperature. Africa will be one of the regions most impacted by the adverse effects of climate change because of high exposure to environmental change, high dependence on agriculture for livelihood and limitations to adapt to these changes.

Anti-platelet resistance

Anti-platelet resistance has been variably defined as clinical or laboratory resistance. In the former, standard drug doses do not prevent a recurrent thrombotic or ischemic event. This clinical resistance, however, is better defined as treatment failure. Multiple pathways are involved in platelet adhesion, activation and aggregation. Therefore, monotherapy directed against a single pathway or receptor, cannot be expected to prevent the occurrence of a thrombotic or ischemic event. A single anti-platelet agent is as such not synonymous with anti-platelet resistance. Laboratory resistance, on the other hand, is defined as failure of standard drug doses to achieve a reduction in platelet aggregation on platelet function tests. In patients on the P2Y12 inhibitor, clopidogrel, the term high platelet reactivity (HPR) to ADP is used to define ‘laboratory resistance’.

A case of narcolepsy type 1 diagnosed by testing CSF orexin: Diagnostic challenges in narcolepsy

The pentad of symptoms recognised in narcolepsy type 1 is excessive daytime sleepiness, cataplexy (sudden attacks of weakness usually triggered by positive emotions), sleep paralysis (inability to move the body on awakening, patients can still move their eyes), sleep hallucinations and disruption of night time sleep. The core symptom is excessive daytime sleepiness. Cataplexy is pathognomonic for narcolepsy type 1. It is important to note that not all patients will present with this pentad of symptoms. In fact, EDS alone can be the only presenting symptom!