Hypertension is identified by the World Health Organization as the leading cause of cardiovascular mortality. And according to the Global Burden of Diseases published in the Lancet, cardiovascular diseases takes the top spot for deaths and diseases each year.
Typically Hypertension is represented by two numbers, the first and often the higher one is the systolic blood pressure which is the arterial pressure when the heart is contracting. And the second, often the lower one is the diastolic pressure which is the arterial pressure when the heart is relaxing or refilling.
Most of the time blood pressure is taken in the brachial artery in the upper arm, because the pressure is usually high there and may give a general representation of blood pressure (although this may not always be the case). The guidelines for determining blood pressure has significantly changed owing to the growing body of evidences showing that even moderately high blood pressures significantly increase the risk of developing heart diseases.
Typically both systolic and diastolic blood pressures climb and fall together but sometimes a patient may have isolated systolic or isolated diastolic hypertension which is an increase on either systolic or diastolic pressure and a normal reading on the other.
Hypertension creates a serious problem for the blood vessels, as it creates a wear and tear effect on the endothelial cells that line them – prolonged, these damages are what eventually leads to diseases such as myocardial infarction (heart attack / failure), aneurysms and stroke.
Hypertension may be separated into Primary Hypertension which includes about 90 percent of all hypertension and has no clear cause and the remaining 10% encompasses Secondary Hypertension. Primary Hypertension or essential hypertension is when pressure in the arteries silently creep up overtime, the risk factors are old age, obesity, salt-heavy diet and a sedentary lifestyle. While humans basically can’t stop aging, the latter three factors may be modified and significantly decrease the risk or reduce hypertension. There is little to no symptoms of primary hypertension, which is why it is aptly named “the silent killer”
About 10% of the time, there is a specific underlying factor for hypertension and this is the secondary type. An example would be a disease that limits the blood flow like atherosclerosis or plaque buildup, vasculitis, aortic dissection and anything that may impede the blood flow in the kidneys. As such Symptoms for secondary hypertension is usually associated with the underlying cause.
The Kidneys are perhaps one of the most important organs in the context of blood pressure. This is due to the The renin–angiotensin system (RAS), or renin–angiotensin–aldosterone system (RAAS), which is a hormone system that regulates blood pressure and fluid and electrolyte balance, as well as systemic vascular resistance. Basically when not enough blood flows through the kidney, the kidney secretes the hormone renin which ultimately helps the kidneys in retaining more water thus increasing the fluid volume and increasing the pressure.
There are other diseases worth mentioning, like Fibromuscular dysplasia, which thickens the large and medium sized blood vessels. Fibromuscular dysplasia may affect the renal arteries in the kidney and trigger the RAS system to produce more renin. Tumors of the adrenal gland may secrete aldosterone and also retain more water in the kidney promoting hypertension.
If the blood pressure gets high really fast, it’s referred to as a hypertensive crisis. This involves a Blood Pressure reading of greater than 180/120mmHg. Hypertensive crisis is further split into two, Hypertensive Urgency and Hypertensive Emergency. Urgency means there hasn’t yet been damage to the end organs like the brain, kidney, heart or lungs, while Emergency shows evidence of damage, producing symptoms like confusion, drowsiness or loss of consciousness, chest pains and difficulty of breathing.
Hypertension, no matter how scary it may seem, has widely available treatments. For one, Lifestyle changes like Diet, Exercise, Stress reduction and quitting vices such as alcohol and tobacco are generally being recommended to all. Antihypertensives are given to supplement it, and are different from individual to individual.
There is a certain fear that Hypertension may take away from some people a chance for a normal life, but this is most often untrue and is merely a matter of perspective. For some, a five peso / day medication to control hypertension is seen as a nuisance, but the regret is felt late when a hundred thousand / day hospital bill comes in due to a heart disease that got furthered by uncontrolled hypertension. Worse, there will be no regrets or anything felt for the matter, with the sudden stoppage of a heartbeat. On a more fortunate note, hypertension is not a hindrance to an active lifestyle, in fact it may actually be a call to one’s body to become more active – of course with the appropriate provisions of one’s physician.
COVID-19 and Hypertension
A July 2020 study publish on the American College of Cardiology entitled “COVID-19 and Hypertension: What We Know and Don’t Know” by Arjun Kanwal, MD and co authors noted that there may be an overrepresentation of hypertension among hospitalized and critically ill COVID-19 patients, so it is uncertain whether this relationship is causal or confounded by age and other co-morbidities associated with hypertension including obesity, diabetes mellitus and chronic kidney disease.
Perhaps an interesting link would be how the SARS-CoV-2 virus binds to ACE2 receptor via its spike (S) protein to allow entry into host cells. Angiotensin converting enzyme or ACE2 is a modulator of the Renin-Angiotensin-Aldosterone-System, a critical neurohormonal pathway that regulates blood pressure and fluid balance. The end product of the RAAS is angiotensin II – which is a key vasoactive hormone that binds to angiotensin II receptor type 1 (AT1) located in the heart, lungs, blood vessels, kidneys, and adrenal glands, and it plays a central role in myocardial hypertrophy and fibrosis, inflammation, vascular remodeling, and atherosclerosis.
ACE2 is expressed in many human tissues including the nasal epithelium, heart, kidneys, and lungs, and inactivates angiotensin II diminishing its vasoconstrictive and myoproliferative effects. When SARS-Cov-2 binds to ACE2 receptors, these down regulates them resulting in the local accumulation of angiotensin II. Local activation of the RAAS is proposed as a mechanism for severe lung injury.
ACE-2 Receptor Agonists
Concerns have been raised about the potential risk associated with RAAS inhibitor drugs. Recent discussions have debated whether ACE-I drugs and Angiotensin Receptor Blocker (ARB) drugs upregulate ACE2 expression thereby facilitating COVID-19 infection or contributing to more severe infection. But it has been revealed that RAAS inhibitor effect on ACE2 levels and tissue activity was inconsistent, with some showing upregulation and others showing no change. Cross-sectional studies of patients exposed to long term RAAS inhibitor therapies revealed that patient’s plasma ACE2 activity was not higher in treated subjects.
With this, Currently, there is no compelling evidence that withdrawal of ACE-I drugs or ARB drugs prevents infection or impacts clinical outcomes – in fact, interruption of these cardioprotective medications including RAAS inhibitors, could lead to clinical decompensation and may lead to increased COVID-19 infection risk.
Most of the peer-reviewed studies published to date have not found higher rates of infection, greater severity of disease, or increased mortality among patients with treated with RAAS inhibitors.
So Basically, for people taking maintenance medications for Hypertension, Diabetes Mellitus and Heart Disease, there is no indication for stopping it, much more now in the pandemic crisis, unless provided by their physician.