At a glance......
- 1 Types
- 2 Causes of Secondary Hypertension
- 3 Symptoms Of Secondary Hypertension
- 4 Diagnosis of Secondary Hypertension
- 5 Treatment of Secondary Hypertension
- 6 Complications
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Secondary hypertension is elevated blood pressure (BP), which is secondary to an identifiable cause. This activity outlines the causes, history, and physical examination findings, diagnostic tests, and management of secondary hypertension, giving particular importance to the role of interprofessional teamwork in managing such patients. It highlights all the clinical clues that can point towards a secondary cause of hypertension.
Secondary hypertension (or, less commonly, inessential hypertension) is a type of hypertension which by definition is caused by an identifiable underlying primary cause. It is much less common than the other type, called essential hypertension, affecting only 5-10% of hypertensive patients. It has many different causes including endocrine diseases, kidney diseases, and tumors. It also can be a side effect of many medications.
Hypertension affects about 30% of adults in the United States. Most cases are due to essential hypertension, i.e., hypertension without an identifiable cause. But, about 5 to 10% of cases of hypertension are due to secondary hypertension.[rx]
Renovascular hypertension – Renovascular hypertension is a condition in which high blood pressure is caused by the kidneys’ hormonal response to the narrowing of the arteries supplying the kidneys.[rx] When functioning properly this hormonal axis regulates blood pressure. Due to low local blood flow, the kidneys mistakenly increase the blood pressure of the entire circulatory system. It is a form of secondary hypertension – a form of hypertension whose cause is identifiable
Other well-known causes include diseases of the kidney. This includes diseases such as polycystic kidney disease which is a cystic genetic disorder of the kidneys, PKD, which is characterized by the presence of multiple cysts (hence, “polycystic”) in both kidneys, can also damage the liver, pancreas, and rarely, the heart and brain.[rx][rx][rx][rx] It can be autosomal dominant or autosomal recessive, with the autosomal dominant form being more common and characterized by progressive cyst development and bilaterally enlarged kidneys with multiple cysts, with concurrent development of hypertension, chronic kidney disease and kidney pain.[rx] Or chronic glomerulonephritis which is a disease characterized by inflammation of the glomeruli, or small blood vessels in the kidneys.[rx][rx][rx]
Hypertension can also be produced by diseases of the renal arteries supplying the kidney. This is known as renovascular hypertension; it is thought that decreased perfusion of renal tissue due to stenosis of a main or branch renal artery activates the renin-angiotensin system.[rx][rx][rx]
Also, some renal tumors can cause hypertension. The differential diagnosis of a renal tumor in a young patient with hypertension includes Juxtaglomerular cell tumor, Wilms’ tumor, and renal cell carcinoma, all of which may produce renin.[rx]
Hypertension secondary to other renal disorders
- Chronic kidney disease
- Kidney disease / renal artery stenosis – the normal physiological response to low blood pressure in the renal arteries is to increase cardiac output (CO) to maintain the pressure needed for glomerular filtration. Here, however, increased CO cannot solve the structural problems causing renal artery hypotension, with the result that CO remains chronically elevated.
- Renal segmental hypoplasia (Ask-Upmark kidney)
Hypertension secondary to endocrine disorders
- Neurogenic hypertension – excessive secretion of norepinephrine and epinephrine which promotes vasoconstriction resulting from the chronic high activity of the sympathoadrenal system, the sympathetic nervous system, and the adrenal gland. The specific mechanism involved is increased release of the “stress hormones”, epinephrine (adrenaline), and norepinephrine which increase blood output from the heart and constrict arteries. People with neurogenic hypertension respond poorly to treatment with diuretics as the underlying cause of their hypertension is not addressed.[rx]
- Pheochromocytoma – a tumor that results in an excessive secretion of norepinephrine and epinephrine which promotes vasoconstriction
- Hyperaldosteronism (Conn’s syndrome) – idiopathic hyperaldosteronism, Liddle’s syndrome (also called pseudoaldosteronism), glucocorticoid remediable aldosteronism
- Cushing’s syndrome – excessive secretion of glucocorticoids causes the hypertension
A variety of adrenal cortical abnormalities can cause hypertension, In primary aldosteronism, there is a clear relationship between aldosterone-induced sodium retention and hypertension.[rx]
Congenital adrenal hyperplasia, a group of autosomal recessive disorders of the enzymes responsible for steroid hormone production, can lead to secondary hypertension by creating atypically high levels of mineralocorticoid steroid hormones. These mineralocorticoids cross-react with the aldosterone receptor, activating it and raising blood pressure.
- 17 alpha-hydroxylase deficiency causes an inability to produce cortisol. Instead, extremely high levels of the precursor hormone corticosterone are produced, some of which is converted to 11-Deoxycorticosterone (DOC), a potent mineralocorticoid not normally clinically important in humans. DOC has blood-pressure raising effects similar to aldosterone, and abnormally high levels result in hypokalemic hypertension.[rx]
- 11β-hydroxylase deficiency, aka apparent mineralocorticoid excess syndrome, involves a defect in the gene for 11β-hydroxysteroid dehydrogenase, an enzyme that normally inactivates circulating cortisol to the less-active metabolite cortisone. At high concentrations cortisol can cross-react and activate the mineralocorticoid receptor, leading to aldosterone-like effects in the kidney, causing hypertension. This effect can also be produced by prolonged ingestion of licorice (which can be of potent strength in licorice candy), by causing inhibition of the 11β-hydroxysteroid dehydrogenase enzyme and likewise leading to secondary apparent mineralocorticoid excess syndrome.[rx][rx][rx] Frequently, if licorice is the cause of the high blood pressure, a low blood level of potassium will also be present.[rx] Cortisol-induced hypertension cannot be completely explained by the activity of Cortisol on Aldosterone receptors. Experiments show that treatment with Spironolactone (an inhibitor of the aldosterone receptor), does not prevent hypertension with excess cortisol. It seems that inhibition of nitric oxide synthesis may also play a role in cortisol-induced hypertension.[rx]
Yet another related disorder causing hypertension is glucocorticoid remediable aldosteronism, which is an autosomal dominant disorder in which the increase in aldosterone secretion produced by ACTH is no longer transient, causing of primary hyperaldosteronism, the Gene mutated will result in an aldosterone synthase that is ACTH-sensitive, which is normally not.[rx]rx][rx][rx][rx] GRA appears to be the most common monogenic form of human hypertension.[rx]
Another adrenal-related cause is Cushing’s syndrome which is a disorder caused by high levels of cortisol. Cortisol is a hormone secreted by the cortex of the adrenal glands. Cushing’s syndrome can be caused by taking glucocorticoid drugs, or by tumors that produce cortisol or adrenocorticotropic hormone (ACTH).[rx] More than 80% of patients with Cushing’s syndrome develop hypertension.,[rx] which is accompanied by distinct symptoms of the syndrome, such as central obesity, lipodystrophy, moon face, sweating, hirsutism, and anxiety.[rx]
Neuroendocrine tumors are also a well-known cause of secondary hypertension. Pheochromocytoma[rx] (most often located in the adrenal medulla) increases secretion of catecholamines such as epinephrine and norepinephrine, causing excessive stimulation of adrenergic receptors, which results in peripheral vasoconstriction and cardiac stimulation. This diagnosis is confirmed by demonstrating increased urinary excretion of epinephrine and norepinephrine and/or their metabolites (vanillylmandelic acid).
Other secondary hypertension
- Hormonal contraceptives
- Neurologic disorders
- Obstructive sleep apnea
- Licorice (when consumed in excessive amounts)
- Pregnancy: unclear cause.
- Cancers: tumors in the kidney can operate in the same way as kidney disease. More commonly, however, tumors cause inessential hypertension by ectopic secretion of hormones involved in the normal physiological control of blood pressure.
- Drugs: In particular, alcohol, nasal decongestants with adrenergic effects, NSAIDs, MAOIs, adrenoceptor stimulants, and combined methods of hormonal contraception (those containing ethinylestradiol) can cause hypertension while in use.
- Heavy alcohol use
- Steroid use
- Nicotine use.[rx]
- Malformed aorta, slow pulse, ischemia: these cause reduced blood flow to the renal arteries, with physiological responses as already outlined.
- Coarctation of the aorta
- Anemia: unclear cause.
- Fever: unclear cause.
- Whitecoat hypertension, that is, elevated blood pressure in a clinical setting but not in other settings, probably due to the anxiety some people experience during a clinic visit.
- Perioperative hypertension is the development of hypertension just before, during or after surgery. It may occur before surgery during the induction of anesthesia; intraoperatively e.g. by pain-induced sympathetic nervous system stimulation; in the early postanesthesia period, e.g. by pain-induced sympathetic stimulation, hypothermia, hypoxia, or hypervolemia from excessive intraoperative fluid therapy; and in the 24 to 48 hours after the postoperative period as fluid is mobilized from the extravascular space. In addition, hypertension may develop perioperatively because of the discontinuation of long-term antihypertensive medication.[rx]
Causes of Secondary Hypertension
Secondary hypertension is elevated blood pressure (BP), which is secondary to an identifiable cause. Since its prevalence is relatively low, performing routine evaluations in every case of hypertension is not cost-effective and is also time-consuming. However, one must be aware of clinical clues that could suggest a secondary cause of hypertension. The clinical clues to look out for that could be suggestive of a secondary cause of hypertension are as follows[rx]
- Diabetes complications (diabetic nephropathy) – Diabetes can damage your kidneys’ filtering system, which can lead to high blood pressure.
- Polycystic kidney disease – In this inherited condition, cysts in your kidneys prevent the kidneys from working normally and can raise blood pressure.
- Glomerular disease – Your kidneys filter waste and sodium using microscopic filters called glomeruli that can sometimes become swollen. If the swollen glomeruli can’t work normally, you may develop high blood pressure.
- Renovascular hypertension – This type of high blood pressure is caused by narrowing (stenosis) of one or both arteries leading to your kidneys.
Resistant hypertension, i.e., persistent blood pressure greater than 140/90 mm Hg despite using three anti-hypertensives from different classes, that includes a diuretic, all at adequate doses.
Increased lability or acute rise in blood pressure in a patient who had previously stable pressures.
Hypertension that develops in non-black patients less than 30 years of age, who do not have any other risk factors for hypertension, e.g., obesity, family history, etc.
Patients with severe hypertension (BP greater than 180/110 mm Hg) and patients with end-organ damage like acute kidney injury, neurological manifestations, flash pulmonary edema, hypertensive retinopathy, left ventricular hypertrophy, etc.
Hypertension is associated with electrolyte disorders like hypokalemia or metabolic alkalosis
Age of onset of hypertension before puberty.
Non-dipping or reverse dipping presents while monitoring 24-hour ambulatory blood pressure. (Normally, the blood pressure at night is lower than the blood pressure during the day, i.e., there is a ‘dip’ in blood pressure at night. The absence of this ‘dip’ or ‘reverse dipping,’ i.e., ‘dip’ present during the day instead of at night can be suggestive of a secondary cause of hypertension).
The etiology of secondary hypertension is varied. The causes subdivide into the following four categories:
- A. Renal causes: Among these, the major categories are renal parenchymal disease (which includes chronic kidney disease and polycystic kidney disease) and reno-vascular disease (which includes renal artery stenosis and fibromuscular dysplasia).
- B. Endocrine causes – Primary aldosteronism, Cushing syndrome/disease, hyperthyroidism, hypothyroidism, hyperparathyroidism, pheochromocytoma including drug-mediated pheochromocytoma crisis,[rx] acromegaly, congenital adrenal hyperplasia.
- C. Vascular: Coarctation of the aorta.
- D. Other: Obstructive sleep apnea, drug-induced hypertension, pregnancy, scleroderma.
Drug-induced hypertension is a significant cause of secondary hypertension. Hence, it is essential to look at the patient’s medication list. Following are the drugs that can cause hypertension[rx]:
Non-steroidal anti-inflammatory drugs, acetaminophen, and aspirin are the commonest implicated drugs in the worsening of blood pressure control due to their widespread use
Drugs used to treat attention-deficit/hyperactivity disorder(ADHD): Methylphenidate, amphetamine, dexmethylphenidate, and dextroamphetamine
Anti-depressants: Monoamine oxidase inhibitors, tricyclic antidepressants, and serotonin-norepinephrine reuptake inhibitors
Atypical antipsychotics like clozapine and olanzapine
Decongestants that have phenylephrine or pseudoephedrine
Herbal supplements like St John wort, ephedra, and yohimbine
Systemic corticosteroids like dexamethasone, methylprednisolone, prednisone, prednisolone, and fludrocortisone
Mineralocorticoids like carbenoxolone, licorice, 9-alpha fludrocortisone and ketoconazole
Estrogens, androgens, and oral contraceptives
Immunosuppressants like cyclosporine
Chronic recombinant human erythropoietin
Recreational drugs: cocaine, methamphetamine, MDMA, bath salts
Chemotherapeutic agents like gemcitabine (which causes microvascular injury)
Symptoms Of Secondary Hypertension
The main symptoms of Secondary hypertension are rapidly increasing blood pressure of 180/120 or higher and signs of organ damage. Usually, the damage happens to the kidneys or the eyes.
Other symptoms depend on how the rise in blood pressure affects your organs. A common symptom is bleeding and swelling in the tiny blood vessels in the retina. The retina is the layer of nerves that line the back of the eye. It senses light and sends signals to the brain through the optic nerve, which can also be affected by malignant hypertension. When the eye is involved, can secondary hypertension cause changes in vision.
Other symptoms of malignant hypertension include
- Pheochromocytoma – Sweating, increased frequency or force of heartbeats, headache, anxiety
- Cushing’s syndrome – Weight gain, weakness, abnormal growth of body hair or loss of menstrual periods (in women), purple striations (lines) on the skin of the abdomen
- Thyroid problems – Fatigue (tiredness), weight gain or weight loss, intolerance to heat or cold
- Conn’s syndrome or primary aldosteronism – Weakness due to low levels of potassium in the body
- Obstructive sleep apnea – excessive fatigue or sleepiness during daytime, snoring, pauses in breathing during sleep
- Change in mental status, such as anxiety, confusion, decreased alertness, decreased ability to concentrate, fatigue, restlessness, sleepiness, or stupor
- Chest pain (feeling of crushing or pressure)
- Nausea or vomiting
- Numbness of the arms, legs, face, or other areas
- Reduced urine output
- Shortness of breath
- Weakness of the arms, legs, face, or other areas
- Blurred vision
- Chest pain (angina)
- Difficulty breathing
- Numbness in the arms, legs, and face
- Severe headache
- Shortness of breath
In rare cases, secondary hypertension can cause brain swelling, which leads to a dangerous condition called hypertensive encephalopathy. Symptoms include:
- Changes in mental status
- Headache that continues to get worse
- Nausea and vomiting
Diagnosis of Secondary Hypertension
Obtaining a complete history and performing a good physical exam is very important when trying to find the underlying cause of hypertension. The following history and physical exam findings point towards a specific cause of secondary hypertension:
Snoring, obesity, and daytime sleepiness could be indicative of obstructive sleep apnea.
History of renal insufficiency, atherosclerotic cardiovascular disease, edema may warrant further evaluation of chronic kidney disease (renal parenchymal disease).
History of recurrent urinary tract infections, kidney stones, acute/chronic abdominal/flank pain, hematuria, progressive renal failure may point towards autosomal dominant polycystic kidney disease (renal parenchymal disease).
A systolic/ diastolic abdominal bruit is audible in reno-vascular disease.
Use of sympathomimetics, acute stress, perioperative setting, tachycardia could all be in the context of excess catecholamines.
Decreased or delayed femoral pulses are seen in coarctation of the aorta.
Weight gain, fatigue, weakness, hirsutism, amenorrhea, moon facies, dorsal hump, purple striae, and truncal obesity present in Cushing syndrome/disease.
Paroxysmal hypertension, headaches, diaphoresis, palpitations, and tachycardia are features in pheochromocytoma.
Fatigue, weight loss, hair loss, diastolic hypertension, and muscle weakness are seen in hypothyroidism.
Heat intolerance, weight loss, palpitations, systolic hypertension, exophthalmos, tremor, and tachycardia will occur in hyperthyroidism.
Kidney stones, osteoporosis, depression, lethargy, and muscle weakness present in hyperparathyroidism.
Headaches, fatigue, visual problems, enlargement of the hands, feet, and tongue are features in acromegaly.
Heartburn, Raynaud phenomenon, nail pitting on the exam may be suggestive of scleroderma.
Lab Test and Imaging
Laboratory tests and imaging modalities also help in diagnosing secondary hypertension. Some of the findings on common tests that can create suspicion for an underlying cause of hypertension are as follows:
Basic Metabolic Panel (BMP) – Hypokalemia presents in primary hyperaldosteronism and Cushing syndrome/disease. Also seen on the BMP in primary hyperaldosteronism, is metabolic alkalosis and hypernatremia. Blood urea nitrogen (BUN) and creatinine become elevated in renal parenchymal disease.
Complete blood count (CBC) – Polycythemia can be present in obstructive sleep apnea.
Urine analysis – Proteinuria can be a feature in renal parenchymal disease.
Chest X-Ray in coarctation of aorta shows inferior rib notching and a figure of 3 sign (abnormality of the contour of the aorta).
Upon establishing suspicion for a particular cause based on history, physical exam findings, and common laboratory tests, certain tests can be used to specifically rule out or rule in a cause of secondary hypertension. They are as follows:
Obstructive sleep apnea (OSA) – Polysomnography (preferably in-laboratory polysomnography) is the diagnostic study of choice when there is a suspicion of obstructive sleep apnea.
Primary hyperaldosteronism – A plasma aldosterone to renin ratio greater than 30, points towards a diagnosis of primary aldosteronism. A CT scan of the abdomen is also done to look for the presence of adenomas or hyperplasia of the adrenal glands.
Renal parenchymal disease – A decreased creatinine clearance occurs in renal parenchymal disease. Renal ultrasonography can be further used to determine the cause for the decreased creatinine clearance. Multiple cysts demonstrate in polycystic kidney disease, and a small contracted kidney is a feature in chronic kidney disease. Genetic testing can also be useful in ADPKD.
Reno-vascular disease – Magnetic resonance angiography/CT angiography/doppler of renal arteries can all be used to look for the presence of stenosis of the renal arteries. Other tests that can be useful are captopril-augmented radioisotopic renography and renal arteriography.
Excess catecholamine use – If the patient is normotensive in the absence of high catecholamines, it rules out excess catecholamines as the cause.
Coarctation of the aorta – Doppler or CT imaging of the aorta will show a narrowing of the aorta. Echocardiography is another modality of choice.
Cushing syndrome/disease – Overnight 1 mg dexamethasone-suppression test and adrenocorticotropic hormone can help diagnose Cushing’s disease and syndrome.
Pheochromocytoma – Urinary catecholamine metabolites (vanillylmandelic acid, metanephrines, normetanephrine) become elevated in pheochromocytoma.
Hyper/hypothyroidism – Serum thyroid-stimulating hormone, thyroxine, and triiodothyronine levels help to diagnose hyperthyroidism and hypothyroidism.
Hyperparathyroidism – Serum calcium and parathyroid hormone levels help in the diagnosis of hyperparathyroidism.
Acromegaly – Elevated growth hormone level can point towards acromegaly.
Scleroderma/ scleroderma renal crisis – Thrombotic microangiopathy, autoantibodies against RNA polymerase III, positive antinuclear antibody (ANA) will present in scleroderma.
Electrocardiogram (ECG or EKG) – This painless noninvasive test records the electrical signals in your heart. You might have this test if your doctor thinks a heart problem might be causing your secondary hypertension.
Ultrasound of your kidneys – Many kidney conditions are linked to secondary hypertension. In this noninvasive test, a technician moves a small, hand-held device called a transducer over the area to be tested. The transducer sends sound waves into your body, collects the ones that bounce back and sends them to a computer, which creates images of your kidneys.
Treatment of Secondary Hypertension
Management of secondary hypertension comprises of adequate control of blood pressure with antihypertensive drugs and addressing the secondary causes mentioned above. This section briefly discusses the management of the more common causes of secondary hypertension, viz: renal parenchymal disease, renovascular hypertension, primary hyperaldosteronism, obstructive sleep apnea, drug-induced hypertension, and pregnancy.
A. Renal parenchymal disease
- Renal parenchymal disease-causing hypertension mainly involves chronic kidney disease (CKD) and autosomal dominant polycystic kidney disease (ADPKD).
- i. Management of chronic kidney disease comprises of treating the reversible causes responsible for causing CKD (e.g., treating hypovolemia with fluids, avoid nephrotoxin use, relieve urinary tract obstruction) and slowing the rate of progression of the disease. To slow the rate of progression, adequate blood pressure control, decreasing urine protein, glycemic control, lifestyle changes like dietary protein restriction, and smoking cessation help. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) are the best anti-hypertensives to use in proteinuric CKD. Bicarbonate use in patients with chronic metabolic acidosis slows progression to end-stage renal disease.[rx]
- ii. Patients with ADPKD eventually require renal replacement therapy. Before that stage reached, hypertension management is with anti-hypertensives: ACE inhibitors or ARBs and sodium restriction. Tolvaptan is an option in patients who are at high risk for progression to CKD. It decreases the rate of estimated glomerular filtration rate decline.[rx]
B. Renovascular hypertension
- Management of renovascular hypertension (i.e., renal artery stenosis from either atherosclerotic disease or fibromuscular dysplasia) divides into medical therapy and revascularization. Medical therapy involves the use of anti-hypertensives to control blood pressure and in the case of atherosclerotic disease, the use of antiplatelets, statins, diet, and lifestyle changes. ACE inhibitors and ARBs are the anti-hypertensives of choice. Other anti-hypertensives that are treatment options are calcium channel blockers and thiazide diuretics.
- Revascularization is usually done by percutaneous angioplasty with stenting of the renal artery. Surgery (which frequently includes aorto-renal bypass or sometimes removal of the ‘pressor’ kidney) is only for patients with complex anatomy.
In the following patients, revascularization may be more beneficial than medical therapy alone
Patients with recurrent flash pulmonary edema
Failure or intolerance to optimal medical treatment
Unexplained, progressive, a decline in renal function,
Recent initiation of dialysis in a patient with suspected renal artery stenosis
An acute increase in creatinine after medical therapy and in patients with a renal resistive index of less than 80 mmHg on Doppler
C. Primary hyperaldosteronism
- Unilateral primary hyperaldosteronism (e.g., unilateral adrenal hyperplasia or aldosterone-producing adenoma) gets treated with unilateral laparoscopic adrenalectomy. If the patient is not a surgical candidate or a patient has bilateral adrenal disease, then medical management with a mineralocorticoid receptor antagonist is recommended- with spironolactone being the primary agent and eplerenone being the alternative.[rx]
D. Obstructive Sleep Apnea
- Continuous positive airway pressure (CPAP) therapy is the mainstay of treatment for OSA. To note, however, lifestyle modifications like weight loss, along with usage of CPAP have a synergistic effect on lowering blood pressure and are better than either intervention alone.[rx]
- An alternative to CPAP is oral appliances, used in mild to moderate OSA, which are non-inferior to CPAP in the reduction of blood pressure and may even help with better compliance in patients. In patients refractory to the above treatment, few upper airway surgeries can be performed to help with symptoms and reduction in blood pressure, like uvulopalatopharyngoplasty (UPPP) in adults and tonsillectomy and adenoidectomy in children. Along with these, anti-hypertensive drugs also help, particularly the ones that modulate the renin-angiotensin system (ACE inhibitors, ARBs, aldosterone antagonists, and beta-blockers are the best options).[rx]
E. Drug-induced hypertension
- In drug-induced hypertension, upon identification of the culprit drug, the management is to withhold it and look for improvement.
- Hypertension in pregnancy comprises chronic hypertension, gestational hypertension, pre-eclampsia, and eclampsia. Chronic hypertension is when hypertension occurs before pregnancy or before 20 weeks of gestation, whereas the other three occur after 20 weeks. Pre-eclampsia is associated with proteinuria, and eclampsia is associated with seizures.
- Interventions for hypertension in pregnancy are lifestyle modifications and anti-hypertensives. The anti-hypertensives commonly used in pregnancy are labetalol, nifedipine, and methyldopa.
- In cases of severe hypertension (severe preeclampsia, eclampsia, and HELLP syndrome), the standard of care is delivered, especially after 37 weeks of gestation. If an acute decrease in blood pressure is required, intravenous labetalol or intravenous hydralazine are options. Magnesium sulfate prevents seizures.[rx][rx]
Blood Pressure Goals
SHEP and HYVET trials have shown significant benefits of antihypertensive treatment in patients with the goal of SBP <150 mmHg[rx].
The VALsartan in Elderly Isolated Systolic Hypertension (VALISH) trial showed no significant difference in the primary outcome of sudden death, fatal or nonfatal myocardial infarction and stroke, heart failure death, or other cardiovascular death among patients with strict (< 140 mmHg) and moderate (140 to 150 mmHg) SBP control[rx].
However, the VALISH trial was underpowered due to the low number of events.
Hence, the optimal SBP in patients with hypertensive disorder remained a controversial topic.
The most recent Systolic Blood Pressure Intervention Trial (SPRINT) has shown that intensive SBP target of < 120 mmHg improved the cardiovascular outcomes and the overall survival compared to the standard SBP target of 135 to 139 mmHg[rx].
However, aggressive SBP lowering may be harmful in the elderly and incite more adverse effects such as hypotension, end-organ hypoperfusion (causing acute kidney injury, and intracranial hypoperfusion which may link to cognitive decline), and polypharmacy.
It is suggested that a goal blood pressure of < 130/80 mmHg is appropriate as long as the patient tolerates it.
Otherwise, < 140/90 mmHg is considered reasonable in patients who are in the elderly population and patients with labile blood pressure or polypharmacy.
Management strategies should always be patient-centered, with the aim of optimizing blood pressure control and avoiding polypharmacy, especially in the elderly.
Various studies have shown a J-curve association between blood pressure with risk of myocardial infarction and death.
As myocardial perfusion occurs mainly during diastole, an excessive drop in DBP may increase the risk of cardiovascular disease and death.
You may also need to make some lifestyle changes as part of your ISH treatment plan. These can include:
- Losing weight. This can help lower your blood pressure. In fact, for every two pounds you lose, you could lower your blood pressure by about 1 mm Hg.
- Eating a heart-healthy diet. You should also aim to reduce the amount of sodium in your diet. Consider the DASH diet, which emphasizes eating:
- whole grains
- low-fat dairy products
- Exercising. Not only can exercise help you lower your blood pressure, but it can help you control your weight and stress levels. Aim to perform some sort of aerobic exercise for at least 30 minutes most days of the week.
- Decreasing alcohol consumption. Healthy alcohol intake is one drink per day for women and two per day for men.
- Quitting smoking. Smoking can raise your blood pressure and also contribute to a variety of other health problems.
- Managing stress. Stress can raise your blood pressure, so finding ways to relieve it are important. Examples of techniques to help lower stress are meditation and deep breathing exercises.
Secondary hypertension can worsen the underlying medical condition you have that’s causing your high blood pressure. If you don’t receive treatment, secondary hypertension can lead to other health problems, such as:
- Damage to your arteries. This can result in hardening and thickening of the arteries (atherosclerosis), which can lead to a heart attack, stroke, or other complications.
- Aneurysm. Increased blood pressure can cause your blood vessels to weaken and bulge, forming an aneurysm. If an aneurysm ruptures, it can be life-threatening.
- Heart failure. To pump blood against the higher pressure in your vessels, your heart muscle thickens. Eventually, the thickened muscle may have a harder time pumping enough blood to meet your body’s needs, which can lead to heart failure.
- Weakened and narrowed blood vessels in your kidneys. This can prevent these organs from working properly.
- Thickened, narrowed, or torn blood vessels in the eyes. This can result in vision loss.
- Metabolic syndrome. This syndrome is a cluster of disorders of your body’s metabolism — including increased waist circumference, high triglycerides, low high-density lipoprotein (HDL) cholesterol (the “good” cholesterol), high blood pressure, and high insulin levels. If you have high blood pressure, you’re more likely to have other components of metabolic syndrome. The more components you have, the greater your risk of developing diabetes, heart disease, or stroke.
- Trouble with memory or understanding. Uncontrolled high blood pressure also may affect your ability to think, remember and learn. Trouble with memory or understanding concepts is more common in people who have high blood pressure.