5 things we now know about atrial fibrillation

Disturbed Blood Flow Can Damage The Vessel Wall In Cases Of Aortic Dilation

Abnormal blood flow in the aorta is linked to inflammation and breakdown of the vessel wall in conditions where the aorta is dilated. This is shown in a study led by researchers at Linköping University. The findings can contribute to better diagnosis and open up new ways to assess the risk of serious and usually fatal complications, such as rupture of the aorta.

All blood in the body passes through the heart about once a minute. With every heartbeat, blood from the heart is pumped up into the aorta.

Dilation can occur in all parts of the aorta. It is unclear exactly how this happens, but one explanation may be weakening of the connective tissue in the vessel wall. Factors such as elevated blood pressure, age and various hereditary conditions increase the risk. A person affected by aortic dilation usually does not notice anything. But more and more people with aortic dilation are being discovered by healthcare -- often by chance.

"In healthcare, we're doing more and more imaging where we look at, for example, the heart or lungs, and then we can find that the patient's aorta is a little larger than normal in some parts. There's a need for more tools to guide doctors on how to handle these patients. In a minority of them, the aorta will unfortunately dilate more, and, in the worst case, the aorta will rupture, which is usually fatal," says Filip Hammaréus, PhD student at the Department of Health, Medicine and Caring Sciences at Linköping University and intern physician at Ryhov County Hospital in Jönköping.

Most people with aortic dilation are offered regular surveillance of the aortic diameter -- the larger the diameter, the higher the risk. Sometimes the aorta is operated on preventively to avoid acute complications, but it can rupture before dilation has become so pronounced that surgery is considered appropriate. At the same time, many examinations are made of people whose aortic diameter does not change. New methods for early identification of patients at elevated risk of growth could contribute to more individualised and cost-effective care. Therefore, the researchers behind the current study, published in the journal European Heart Journal -- Cardiovascular Imaging, are investigating new methods for understanding both the risk and the condition itself.

"We can be onto something new, which can say something more about the severity of the disease than what the aortic diameter shows," says Petter Dyverfeldt, professor at Linköping University and affiliated to the Center for Medical Image Science and Visualization, who has led the study.

When blood is pushed out of the heart into the aorta, a frictional force occurs between the flowing blood and the vessel wall. This is important for a type of cell that is located in the vessel wall and can sense blood flow. When the frictional force is normal, the cells tend to be healthy. However, if the friction significantly changes direction, or becomes very low or abnormal in other ways, there seems to be a signalling into the vessel wall that can eventually lead to a weakening.

Blood flow through the body's large vessels and in the heart can be measured and visualised with magnetic resonance imaging, using an advanced technology called 4D flow MRI that is available in a small number of hospitals. This gives the researchers a picture of how blood flow affects the vessel wall.

In the current study, the researchers have carried out such measurements and also measured various proteins in the blood. It turned out that there existed interesting relationships between the effect of blood flow on the aortic wall and various proteins that relate to inflammation and the build-up and degradation of connective tissue.

"We see that in patients with dilated aorta, abnormal blood flow dynamics are associated with increased inflammation and turnover of connective tissue -- something we believe can reflect processes in the vessel wall. This seems reasonable based on the mechanisms that have been shown in previous research, but it's completely new to show the connections in the way we do now using a combination of magnetic resonance imaging and blood samples," says Filip Hammaréus.

The findings strengthen previous research, but also bring new insights.

"What's interesting about the findings in our study is that the measures of how blood flow affects the aortic wall were not linked to the diameter of the aorta. So, the traditional measure that's often used in healthcare was not part of the relationship we see in the study between abnormal blood flow, inflammation and breakdown of the vessel wall," says Petter Dyverfeldt.

The study was conducted on 47 men and women who participated in the Swedish CArdioPulmonary bioImage study (SCAPIS) and whose aortic diameter was over 40 mm. They were compared with 50 control subjects who were matched by sex and age.

The research has been funded with support from, among others, ALF Grants, Region Östergötland, Linköping University, Region Jönköping (Futurum) and the Swedish Research Council. The main funder of SCAPIS is the Swedish Heart-Lung Foundation.

Facts:

The aorta is shaped like a walking stick with a curved handle. From the heart, the aorta goes up into a bend (the "handle") and from there the long part of the vessel passes down through the chest to the abdomen.

It is easier to find dilated aortas, or aneurysms, on the part of the aorta located in the abdomen. In Sweden, all men over the age of 65 are offered screening for abdominal aortic aneurysm. In the current study, the researchers focused on the dilation of another part of the aorta -- the very first part after the heart -- that is difficult to find with ultrasound and is not included in the screening programme.

Knowns And Unknowns In Subclinical Aortic Valve Thrombosis

Bioprosthetic valve thrombosis found on imaging—with no symptoms reported by the patient—presents a conundrum for clinicians. What are the odds a given case will ultimately impact hemodynamics, potentially impairing durability, and what if anything should be done?

A new review, published online recently ahead of print in Circulation: Cardiovascular Interventions, sums up the literature on incidence, mechanism, diagnosis, and optimal management.

Lead author Kalyan R. Chitturi, DO (MedStar Washington Hospital Center, Washington, DC), speaking with TCTMD, said he and his colleagues wanted to pull together what's known—and what's not—about the topic in both transcatheter and surgical valves.

The review comes on the backdrop of advances in cardiac computed tomography angiography (CCTA) as well as trial designs that increasingly include standardized CT surveillance. Both have raised the question of how to handle subclinical bioprosthetic valve thrombosis, namely hypoattenuated leaflet thickening (HALT) and reduced leaflet motion (RLM), when it's detected. Stroke risk is the more immediate concern, though these CT findings may also raise flags for diminishing valve performance over the ensuing years or decades.

Jonathon Leipsic, MD (University of British Columbia/St. Paul's Hospital, Vancouver, Canada), said "it's one of more thoughtful reviews I've seen on the subject," in that it covers the work done by VARC-3 in characterizing valve thrombosis as well as insight from mechanistic, observational, and randomized studies.  "It's a very nice go-to piece for people in the broader community that really want a soup-to-nuts [summary] of what we've learned" since the first reports on the topic emerged in 2015.

Gilbert Tang, MD (Mount Sinai Health, New York, NY), said that the "no one knows" how much subclinical valve thrombosis truly matters. Even in low-risk patients, these cases "come and go," he said. "The rate is definitely higher than what we probably should be seeing—it's over 20%—[but] some disappear, and some appear. So we just don't know what kind of conditions, whether it's patient, anatomic, device-related, or procedure factors, we can pinpoint to better prevent this from happening."

For clinicians wading through the evidence base, it's helpful to have all the information in one document, Leipsic and Tang agreed. The review offers an algorithm, for instance, with guidance on how to diagnose and manage bioprosthetic valve thrombosis, which Chitturi noted is especially helpful in subclinical cases, "where the area is much more gray."

How Much Does HALT Matter?

With follow-up from low-risk TAVI trials now available beyond 5 years, "we're seeing that the whole idea of management of HALT really needs a paradigm shift in thinking," said Chitturi. Up-front prophylaxis with anticoagulant therapy appears to offer "little to no benefit in terms of stroke prevention [but] a real risk of bleeding," Chitturi said. The data suggest "maybe we were too aggressive with stroke prevention [through] anticoagulation."

Now, with evidence from GALILEO and other studies, there's a shift away from universally giving anticoagulation to all TAVI patients. When patients have an indication for anticoagulation, studies suggest a direct oral anticoagulant may be better than a vitamin K antagonist.

Prophylactic anticoagulation "can increase undue harm with bleeding, especially in patients who are at high surgical risk and elderly," Tang told TCTMD. That said, it "may be reasonable" to offer 3 months of anticoagulation to younger patients who are better able to tolerate it, he added. For those without an indication for anticoagulation, though, the POPular TAVI trial shows a single antiplatelet is sufficient.

When subclinical cases do occur, they don't always progress to clinical issues and sometimes can resolve. In the PARTNER 3 CT substudy "a lot of the low-grade HALT disappeared upon longer-term follow-up up to a year. But then, within that year, new cases of HALT developed," Chitturi pointed out. "That shows that HALT is a dynamic process. It's still poorly understood." The Evolut Low Risk trial stands as another example: nearly three in 10 patients had HALT at 1 year, the review notes, but less than half a percent had clinical valve thrombosis by 3 years.

Both of these low-surgical-risk trials of TAVI versus SAVR had protocols for CT surveillance, said Chitturi. Because of this, "we were also able to see that there was actually a higher rate of subclinical leaflet thrombosis after bioprosthetic SAVR than had previously been reported in the literature. It was very underreported. Now we have a greater understanding that it's an entity that not only affects transcatheter heart valves, but also bioprosthetic surgical valves, and may have an impact on their durability long term as well."

Once higher gradients are in play, whether that "portends a worse clinical outcome in terms of bioprosthetic valve dysfunction and failure is to be determined," he added. "It is a controversial area. If we extrapolate from the surgical literature, it may play a role, but the jury is still out. We do not know."

With HALT, "we still don't entirely understand whether this is important to cover and whether it's clinically relevant or not," Leipsic agreed, noting that evidence is currently mixed on whether HALT is associated with higher risk of future degeneration. "But I think the field continues to want to understand." If there is a link, he added, then "does identifying it early and treating it prevent that progression to valve degeneration? Or is it already too late?"

Leipsic pointed out that half the time HALT does go away on its own. Going forward, it will be important to track how various strategies for addressing the condition affect longer-term outcomes, he said.

Along with the algorithm, the review does offer some other advice.

"Major advances over the past 5 years in diagnosing and understanding the clinical implications of subclinical leaflet thrombosis have informed a more conservative approach to surveillance and treatment. Based on the best available evidence, patients who have undergone TAVR or bioprosthetic SAVR should undergo focused and comprehensive clinical assessment and evaluation of bioprosthetic valve function with [transthoracic echocardiography; TTE] at their follow-up visits," the authors write.

CCTA, on the other hand, "should be reserved for patients with clinical thromboembolism or abnormal hemodynamics on TTE due to the harm of unnecessary anticoagulation outweighing any treatment benefit for low-grade HALT or RLM," Chitturi and colleagues conclude, saying that therapeutic oral anticoagulants should be reserved for use in severe HALT or RLM with hemodynamic valve deterioration or clinical valve thrombosis.

At this point in time, the best path is annual surveillance with TTE after AVR, Tang also specified. "The cardiologist should do an echo to look for any signs of gradient increase that are unexpectedly high or any kind of change in the valve measurements in terms of leakage. Those are early signs we need to look into further."

When HALT is identified, "there's no consensus right now" about what to do, said Tang. "If there's no change in echo gradients or hemodynamics, I think most people would say, 'Leave it alone.'" But with some early data suggesting the condition could lead to long-term durability issues, a short 1- to 3-month bout of anticoagulation might be helpful as a way to nip it in the bud, he suggested. Whether some aspects of this phenomenon are irreversible, though, remains to be seen.

What Are The End Stages Of Aortic Stenosis?

A number of patients are asymptomatic

Medically reviewed by Anisha Shah, MDMedically reviewed by Anisha Shah, MD

Aortic stenosis occurs when the aortic valve between the heart's left ventricle and the aorta narrows, restricting blood flow. Aortic stenosis can be mild, moderate, or severe, depending on the symptoms.

Often, aortic stenosis causes no symptoms or only mild symptoms until it becomes severe, which is a serious condition that may involve end-of-life considerations if surgical treatment is not an option.

This article discusses end-stage aortic stenosis facts, symptoms, treatment, prognosis, and advance care planning.

Takeaway

Aortic stenosis can be congenital, meaning you're born with the condition. However, it most commonly occurs from calcium buildup or scarring in the aortic valve due to age.

End-Stage Aortic Stenosis: The Facts

There are some facts you should know about end-stage aortic stenosis, such as heart damage, risk factors, and prognosis.

Heart Damage

In end-stage aortic stenosis, the left ventricle has to work harder to pump blood because the aortic valve is narrowed. This can cause the left ventricle wall to thicken, affecting the heart's ability to supply blood to the rest of the body.

Without treatment, aortic stenosis can lead to heart failure, a severe condition in which the heart doesn't pump well enough to supply the body with enough blood and oxygen.

Risk Groups

Aortic stenosis is a progressive condition, but the reasons it progresses are mainly unknown. Risk factors that can be associated with quicker progression or aortic stenosis include:

Prognosis at Diagnosis

Without valve replacement surgery, end-stage aortic stenosis without symptoms (asymptomatic) has a poor long-term survival rate similar to that of some cancers. The one-year survival rate in patients younger than 70 years old with severe aortic stenosis without symptoms is 46% at three years and 37% at four years. The four-year survival rate in patients over 70 years old with severe aortic stenosis without symptoms is 16%.

The average life expectancy for aortic stenosis with symptoms (such as shortness of breath or chest pain) is one to two years without treatment. About one-third of patients with aortic stenosis do not receive valve replacement surgery, which is the only effective treatment for the condition.

Symptoms (or No Symptoms) of End-Stage Aortic Stenosis Takeaway

Aortic stenosis creates a unique heart murmur that changes as the disease progresses. The murmur can typically be heard when a healthcare provider listens to the heart with a stethoscope during a physical exam.

About one-fourth of patients with severe aortic stenosis don't have any symptoms. However, symptoms might be underreported in older adult patients because of other conditions they may have, such as memory issues, degenerative arthritis, and poor mobility.

Severe aortic stenosis can occur without symptoms for years. Unless treated with valve replacement surgery, the likelihood of having no symptoms from severe aortic stenosis is 82% after one year, 67% after two years, and 33% after five years.

Symptoms of aortic stenosis often don't occur until there is severe damage to the heart valve. Symptoms of end-stage aortic stenosis include:

Treatment During End-Stage Aortic Stenosis

Valve replacement surgery is the only treatment that can improve survival and quality of life in those with end-stage aortic stenosis. It is performed through open-heart surgical aortic valve replacement surgery (SAVR) or minimally invasive transcatheter aortic valve replacement (TAVR).

With TAVR, a new valve is placed inside the diseased valve through a catheter. The procedure has fewer risks and a quicker recovery time than open heart valve replacement surgery. TAVR was first performed only in those with aortic stenosis who were too high risk for open heart surgery, but it is now performed in lower-risk patients as well.

Older patients who are frail or have other conditions such as lung disease, coronary artery disease, or renal (kidney) dysfunction might not be candidates for valve replacement surgery. In these cases, palliative care (specialized care aimed at relieving symptoms) can be used alongside medications and other methods to reduce symptoms and improve quality of life.

Specialists Involved and Hospitalization

If you have end-stage aortic stenosis, your care team will usually include:

If you have valve replacement surgery, it will be performed in a hospital. There, specialists who treat you can include:

An interventional cardiologist or cardiothoracic surgeon

A valve clinic coordinator to help you navigate treatment

A cardiovascular anesthesiologist (gives anesthetic medicines during heart surgery)

Cardiovascular nurses

Tips for Caregivers

One of the challenges in managing end-stage aortic stenosis is ensuring that medical treatment is balanced with supportive care.

At the time of diagnosis of end-stage aortic stenosis, advance care planning and palliative care should be discussed. Even if a patient is a candidate for valve replacement surgery, it's possible the surgery will not go as planned or have complications.

Palliative care is specialized care that can play an essential role in patients with end-stage aortic stenosis at the time of diagnosis and throughout the disease. Advance care planning and palliative care can help:

Reduce caregiver and patient anxiety

Manage patient symptoms

Help caregivers follow patient wishes

Improve communication between patients, caregivers, and families

Provide psychosocial, spiritual, and bereavement support

Summary

Because aortic stenosis often doesn't have symptoms, especially in its early stages, you might not know you have the condition until it's severe. End-stage aortic stenosis can cause serious heart damage and has a limited life expectancy unless valve replacement surgery is performed. Advance care planning should be discussed to benefit the patient and caregivers when end-stage aortic stenosis is diagnosed.

Read the original article on Verywell Health.

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