Chapter 10 Hypertension and stroke
EPIDEMIOLOGY AND AETIOLOGY
Hypertension or high blood pressure (BP) is a sustained rise in resting blood pressure. Persistent systolic blood pressure (≥ 140 mmHg) and diastolic blood pressure (≥ 90 mmHg) is considered ‘hypertension’.1 It is very common, affecting approximately one-third of the population. Hypertension is an important risk factor in coronary heart disease and in cerebrovascular accident or ‘stroke’, and may also lead to kidney failure and left ventricular failure or ‘heart failure’.2,3 Hypertension with no known cause (primary) is the most common (90%), and hypertension with an identified cause (secondary) can be due to kidney disease (the most common cause), coarctation of the aorta, endocrine diseases and pregnancy.1 Diagnosis is by sphygmomanometry, usually over three consecutive visits to a medical doctor.4
Left ventricular hypertrophy usually develops in response to some factor, such as high blood pressure, that requires the left ventricle to work harder. As the workload increases, the walls of the chamber grow thicker, lose elasticity and eventually may fail to pump with as much force as a healthy heart.5 Left ventricular hypertrophy presents with increased risk of heart disease, including heart attack, heart failure, irregular heartbeats (arrhythmia) and sudden cardiac arrest.6
The term ‘stroke’ encompasses a heterogenous group of cerebrovascular disorders. Ischaemic stroke or cerebral infarction accounts for 80–85% of all strokes and typically presents as a sudden, painless, focal neurological deficit with preserved consciousness.1,2 Haemorrhagic stroke accounts for 15–20% of all strokes, and presents as an acute focal neurological deficit, but continues to worsen as the haematoma expands, with headache and altered consciousness resulting.5
RISK FACTORS
Genetics, social behaviour and diet all have a role to play in this multifactorial condition (see Figure 10.1).7 The risk of high blood pressure increases with age, and is more prevalent in middle-aged men and postmenopausal women.8 It develops at an earlier age in black ethnicity than it does in Caucasians and is influenced by family history. Although the long-term effect of stress on blood pressure is not well understood, chronic stress can lead to transient rises of significant hypertension.9 Dietary factors that may affect hypertension include high levels of salt, reduced levels of potassium, and heavy drinking. Apart from alcohol, other social behaviours such as smoking and physical inactivity have long-term detrimental effects on blood pressure.10
CONVENTIONAL TREATMENT
The initial medical treatment in non-life-threatening hypertension centres on weight loss and dietary changes.11 Patients are encouraged to increase the level of fruits and vegetables in their diet, while concurrently reducing salt and alcohol intake. These interventions, combined with regular aerobic exercise, can reduce systolic blood pressure by 6–10 mmHg.13
If the hypertension is high (> 140/90 mmHg) on several occasions or unresponsive to lifestyle modification, then drug therapy is instigated.1 For uncomplicated hypertension, unless there is a contraindication or a specific indication for another drug, then the order of consideration is:
For all patients, treatment aims to reduce BP to < 140/90 mm Hg; for those with a kidney disorder or diabetes, the goal is < 130/80 mm Hg or as near this level as tolerated. Even the elderly and frail can tolerate a diastolic BP as low as 60 to 65 mm Hg well without an increase in cardiovascular events.1
KEY TREATMENT PROTOCOLS
due to differences in the intake of certain nutrients. Sustained raised blood pressure is positively associated with higher sodium, alcohol and protein intakes, and is inversely associated with potassium, calcium and magnesium intake.13 Due to this, dietary and lifestyle measures are of primary focus in treating hypertension.
Stress reduction
The stress response increases sympathetic nervous activity, which can adversely affect the cardiovascular system (see Chapter 15 on adrenal fatigue). Cardiovascular disease is due in part to stress-induced mechanisms mediated primarily through increased adrenergic stimulation.5 These stress-induced mechanisms include elevations in serum lipids, alterations in blood coagulation, atherogenesis, vascular changes in hypertension and myocardial ischaemia.9
It is difficult to quantify the extent to which stress influences cardiovascular health; however, there are causal relationships between stress and pathophysiological behaviours that in turn have detrimental effects on health, including hypertension. A study over 7 years with 6576 subjects clearly indicated that stress led to increased consumption of alcohol, smoking and a reduction in physical activity.14 A small Indian study in 2008 of 77 individuals looked at the short-term effect of a comprehensive but brief lifestyle intervention with yoga on their subjective wellbeing. The group included healthy individuals as well subjects with hypertension, coronary artery disease and diabetes mellitus. The results suggested that the stress management program made an appreciable contribution to primary disease prevention.15
Interventions for coronary heart disease-prone behaviour patterns have proven successful. A large study was found to support the effect of therapeutic lifestyle changes on hypertension (see Table 10.2 at the end of the chapter for a review of the evidence).11 Valeriana officinalis may have a positive effect on anxiety and stress, as well as on vasospastic activity.16 It is believed that the relaxing effect of V. officinalis is related to the level of valerenic acid, a sesquiterpenic acid, which specifically modulates certain GABA-α receptors and activity.17 A 2007 study found ethanolic extracts of valerian to be as effective as nifedipine in their ‘anticoronaryspastic’ activity against cardiovascular disease.18 Another sesquiterpene isolated from Magnolia grandifolia flower petals produced a statistically significant decrease in coronary vascular resistance on the Langendorff isolated perfused heart.19 Passiflora incarnata was as effective as oxazepam in the treatment of generalised anxiety disorder, with low incidence of impairment of job performance20 (see Section 5 on the endocrine system and Section 4 on the nervous system).
Arterial elasticity and integrity
Age-related changes in the arterial system begin in the 1930s and accelerate through midlife.5 Increased collagen deposition and weakened vascular elastin result in altered elasticity, distensibility and dilatation.5 Stiffening of the central arteries results in higher wave velocities and augmentation of systolic arterial pressure.5 In a double-blind, randomised and placebo controlled clinical study, 26 overweight hypertensive patients were given 3 g of omega-3 fish oil daily for 8 weeks.21 After 8 weeks’ follow-up, the large artery elasticity in the fish-oil group, compared with its baseline, had significantly improved. A small study of 28 middle-aged men and women undertaking a randomised, double-blind trial of 400 IU of vitamin E daily for 8 weeks improved arterial compliance by 44% in 12 out of 14 subjects.22 Antioxidants, such as bioflavonoids, enhance endothelial nitric oxide (NO) synthase expression and subsequent NO release from endothelial cells; this is important in arterial vasodilation. Pycnogenol, an extract of bark from Pinus pinaster (French maritime pine) consists of a concentrate of water-soluble polyphenols. Pycnogenol contains the bioflavonoids catechin and taxifolin, as well as phenolcarbonic acids. Pycnogenol augments endothelium-dependent vasodilation by increasing NO production in the vascular wall.23
Dietary flavonoids, such as quercetin and epicatechin, can augment nitric oxide status and reduce endothelin-1 concentrations, and may thereby improve endothelial function.24 Cocoa is rich in plant-derived flavonoids. In the Zutphen Elderly Study, a cohort of 470 elderly men revealed that cocoa intake was inversely related to blood pressure. A small amount of dark chocolate daily (6 g) in the evening significantly reduced mean systolic blood pressure by 2.9 ± 1.6 mmHg and diastolic blood pressure by 1.9 ± 1.0 mmHg.25 Although still debated, a range of potential mechanisms through which flavonols and cocoa might exert their benefits on cardiovascular health include activation of NO and antioxidant anti-inflammatory and antiplatelet effects, which in turn might improve endothelial function, lipid levels, blood pressure, insulin resistance and eventually clinical outcome.25 It was also shown that homocysteine-lowering therapy improved small arterial elasticity in diabetic patients treated with high-dose metformin.26
Magnesium plays a role in a number of chronic disease-related conditions, including hypertension. Magnesium acts as a calcium channel antagonist, stimulates production of vasodilator prostacyclins and nitric oxide and alters vascular responses to vasoactive agonists.27 It may also play a role in metabolic syndrome and raised serum lipid profiles. Interestingly, it has a more profound effect when added to the diet than it does when supplemented.28
Most of the herbal treatments for hypertension probably act as peripheral vasodilators.1 One of the most useful herbs is Crataegus oxyacantha; its leaves, flowers and fruits contain such biologically active substances as flavonoids and catechins, which appear to be related to C. oxyacantha antioxidant effects.29 As well as reducing high blood pressure this herb has a trophic effect on heart muscle.31 Other studies have shown that C. oxyacantha reduces resting heart rate and mean diastolic blood pressure during exercise and increases the perfusion of the myocardium through revascularisation.29 This is important because left ventricular heart failure is often caused by prolonged hypertension.1 In a pilot study where 500 mg of Crataegus oxyacantha extract was taken daily for 10 weeks, there were promising results on the diastolic component of mild hypertension among subjects.30
Vasopressin and diuresis
Diuretics have long been used to treat hypertension in general practice. Technically, a ‘diuretic’ is an agent that increases urine volume, while a ‘natriuretic’ causes an increase in renal sodium excretion. Because natriuretics almost always also increase water excretion, they are usually called diuretics.31 Generally, diuretics should be initiated at the lowest effective dose of the class chosen. Problems that may occur with both short- and long-term use of diuretics include hyponatraemia, hypokalaemia, metabolic alkalosis and increased uric acid levels. Carbohydrate metabolism is frequently disturbed, with resultant hyperglycaemia and insulin resistance.32 A review of the scientific evidence associated with herbal diuretics showed promising results.31 One such herb that exhibits diuretic effects is Taraxacum officinale. It is important that the leaves are used, as they have high levels of potassium.31 The effect of an aqueous extract of Phyllanthus amarus administered intravenously on male normotensive rabbits produced a fall in mean diastolic, systolic and arterial pressure.33 Methyl brevifolincarboxylate isolated from the leaves of Phyllanthus niruri showed a vasorelaxant effect on rat aortic rings. It exhibited slow relaxation activity against norepinephrine-induced contractions of rat aorta with or without endothelium.34 A single oral administration of a 5% aqueous extract of Phyllanthus sellowianus (400 mg/kg body weight) produced significant increases in urinary excretion in test animals.35 Clerodendron trichotomum has been traditionally used for the treatment of hypertension in China, Korea and Japan. An ethanolic extract produced the following phenylpropanoid glycosides: acteoside, leucosceptoside A, martynoside, acteoside isomer and isomartynoside. These glycosides displayed significant angiotensin-converting enzyme inhibition.36
