I am pleased to announce that despite recent Medicare cuts, I have purchased the Advanced Critical Care Assessment equipment which is useful for assessing vascular elasticity and predicting risks of autonomic dysfunction, and orthostatic hypotension, both of which can cause syncope and falls. Although Medicare has various codes for the procedures, in most cases they do not want to cover peforming the testing. However, we have purchased the equipment and will be providing the testing to our patients with risk factors regardless of insurance or Medicare coverage. Below is an article describing how part of the diagnostic testing is being used to guide therapy. If interested in having the test performed, please call the office and ask to have “CAN” testing performed. If you are not a patient of the practice, testing can be arranged on a fee for service basis.
BARCELONA, Spain — An aging population grappling with rising rates of hypertension and other cardiometabolic risk factors should prompt an overhaul of how hypertension is diagnosed and monitored and should spur development of drugs with entirely new mechanisms of action, one expert says. Speaking here at the 2013 International Conference on Prehypertension and Cardiometabolic Syndrome, meeting cochairDr Reuven Zimlichman (Tel Aviv University, Israel) argued that the definitions of hypertension, as well as the risk-factor tables used to guide treatment, are no longer appropriate for a growing number of patients.
“In recent decades, the population has been growing older, and the elderly now make up the biggest group of hypertensive patients. And this will continue to get bigger in the next few years, as we prolong life and people live longer,” he said in an interview with heartwire . This, he continued, has led to burgeoning numbers of patients with isolated systolic hypertension (ISH) whose disease is typically ill-diagnosed and underserved by current therapies.
Whereas classic, diastolic hypertension is caused by humoral changes and excessive vasoconstrictive factors, he explained, isolated systolic hypertension is caused by arterial stiffening. “So we have a growing group of patients with hypertension caused by a different mechanism–arterial stiffness–yet we treat these patients with conventional medications that lower BP.”
Most antihypertensives today work by producing vasodilation or decreasing blood volume and so are ineffective treatments in ISH patients. In the future, he predicts, “we will have to start looking for a totally different medication that will aim to improve or at least to stabilize arterial elasticity: medication that might affect factors that determine the stiffness of the arteries, like collagen, like fibroblasts. Those are not the aim of any group of antihypertensive medications today.”
Taking “Linear Progression” Into Account
Zimlichman also argued that definitions of essential and secondary hypertension have changed very little over the past few decades and have typically only been tweaked up or down related to other CV risk factors. Diastolic hypertension has been the primary goal of treatment, and treatment goals have not adequately taken patient age into account (in whom arterial stiffening plays a larger role), and they have typically relied too heavily on threshold cutoffs, rather than the “linear progression” of risk factors and their impact on organ damage.
“This means that a patient with a systolic BP of 138 mm HG will be classified as normal risk, while the patient who has 142 mm Hg will be classified as hypertensive, despite there being just 4-mm-Hg difference between the two. And we know that if we repeat the measurement we will probably not get the same result,” Zimlichman stated. “What we have to understand is that various patients will need different approaches. So a patient with hypertension but also with additional risk factors like diabetes, dyslipidemia, etc, probably will need to be treated earlier, at lower levels of BP, and we do not always take this into account.”
Existing risk tables incorporate presence or absence of cardiometabolic risk factors but fail to take into account whether elevated lipids or blood pressure or glucose have already had a pathologic effect, he pointed out to heartwire .
For example, “we can see sometimes a patient with diabetes–treated or not treated, compliant or not compliant–who has had diabetes 20 or 30 years with no evidence of end-organ damage at all. And in the opposite group you can have a patient who has diabetes and who within two or three years develops renal failure, microalbuminuria, glycoproteinuria, or severe vascular disease. Those two patients might have similar levels of glucose, of hyperglycemia, but they clearly respond in different ways.’
As such, grading a patient based on a threshold cut point for any given risk factor “doesn’t tell us the whole story, because we have to include the individual response of the patient to various risk factors as well,” he argues. “These are partially incorporated into present guidelines, but not enough.”
Zimlichman believes existing databases could be used to develop algorithms that take this progression of disease into account, in order to better guide hypertension management. He also points out that new ambulatory blood-pressure-monitoring devices also measure arterial elasticity. “Unquestionably, these will improve our ability to diagnose both the status of the arteries and the changes of the arteries with time as a result of our treatment. So if we treat the patient and we see no improvement in arterial elasticity, or the patient is worse, something is wrong, something is not working–either the patient is not taking the medication, or our choice of medication is not appropriate, or the dose is insufficient, etc.”
Predicting End-Organ Damage
Evidence has been mounting that arterial stiffening is a key predictor of future organ damage, Zimlichman said. “I think that a big proportion of cardiologists are not exposed to new information that was published in recent years regarding the evaluation of arterial properties and prediction of events. In this field, there are very important new findings and also implications regarding treatment.”
As researchers learn more about ISH and the role of arterial elasticity, there are larger “more philosophical” questions to be considered, Zimlichman observed.
“We have normograms of how stiff arteries are according to age groups in healthy patients, and we usually compare those values with the values that we measure in patients with problems: metabolic syndrome, hypertension, diabetes, etc. But is stiffening of the arteries a physiological process, part of normal aging, or is it really pathological?”
In the future, Zimlichman envisions drugs that can slow, stop, or reverse arterial stiffening, but this should give some pause for thought. “Imagine somebody who is 80 years old and has, according to age group, so-called ‘normal’ stiffness–will we change the patient’s fate if we improve the status of the arteries at a younger age, even in a ‘normally’ aging subject? Will it prolong life or prevent events? We don’t know.”