Article Figures & Data
Figures
- Figure 1
Effects of statins (hydroxymethylglutarate (HMG) coenzyme A reductase inhibitors) on synthesis of ubiquinone (coenzyme Q10, CoQ10). Between the inhibition of HMG coenzyme A reductase and cholesterol are many intermediate metabolites. By the same action that lowers levels of low-density lipoprotein cholesterol, statins also lower levels of CoQ10; this may lead to mitochondrial dysfunction contributing to myopathy and insulin resistance/diabetes (reproduced by permission of Vanderbilt University Press from: Spence).29
- Figure 2
Detection of microemboli by transcranial Doppler identifies high-risk asymptomatic carotid stenosis. The white arrow in the upper channel shows the M-mode image of a microembolus in the middle cerebral artery ipsilateral to an asymptomatic carotid stenosis; the high-intensity transit signal is seen (white arrow) in the Doppler channel below (reproduced by permission of Wolters Kluver from: Spence JD et al).36
- Figure 3
Microemboli during deployment of a carotid stent. Microemboli during carotid stenting. Showers of emboli commonly (even usually) occur during carotid stenting. Panel A shows microemboli in both middle cerebral arteries while crossing the aortic arch during stenting of a common carotid; panel B shows microemboli in the middle cerebral artery during stenting of the ipsilateral internal carotid artery (courtesy of Dr Claudio Muñoz. Reproduced by permission of Springer to reproduce from: Spence et al).45
- Figure 4
Decline in the risk of carotid occlusion with more intensive medical therapy. Among 3681 patients in the database, the percentage of patients who progressed to occlusion was much higher before 2002; the frequency decreased markedly after implementation in 2002–2003 of more intensive therapy based on plaque measurements. Error bars indicate 95% CI (reproduced by permission of the American Medical Association from: Yang et al).46
Tables
- Table 1
Physiologically individualised therapy* based on renin/aldosterone profile
Primary hyperaldosteronism Liddle's syndrome and variants (renal Na+ channel mutations) Renal/renovascular Renin Low† Low High Aldosterone High† Low High Primary treatment Aldosterone antagonist (spironolactone or eplerenone)
Amiloride for men where eplerenone is not available (rarely surgery)Amiloride Angiotensin receptor blocker or renin inhibitor§ (rarely revascularisation) Reproduced by permission of Elsevier from: Spence.19
*It should be stressed that this approach is suitable for tailoring medical therapy in resistant hypertensives; further investigation would be required to justify adrenalectomy or renal revascularisation.
†Levels of plasma renin and aldosterone must be interpreted in the light of the medication the patient is taking at the time of sampling. In a patient taking an angiotensin receptor blocker (which would elevate renin and lower aldosterone), a plasma renin that is in the low normal range for that laboratory, with a plasma aldosterone in the high normal range, probably represents primary hyperaldosteronism, for the purposes of adjusting medical therapy.
§Angiotensin receptor antagonists are less effective because of aldosterone escape via non-ACE pathways such as chymase and cathepsin.
