Tag: myocardial infarction

Categories : Cardiovascular Disease GenderTags :

Atherosclerosis is a Greater Heart Attack Risk for Women

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Postmenopausal women with atherosclerosis are at higher risk of heart attacks than men of similar age, according to research presented at EACVI 2023, a scientific congress of the European Society of Cardiology (ESC), and published in European Heart Journal – Cardiovascular Imaging. Researchers used imaging techniques to examine the arteries of nearly 25 000 patients and followed them for heart attacks and death.

“The study suggests that a given burden of atherosclerosis is riskier in postmenopausal women than it is in men of that age,” said study author Dr Sophie van Rosendael of Leiden University Medical Centre. “Since atherosclerotic plaque burden is emerging as a target to decide the intensity of therapy to prevent heart attacks, the findings may impact treatment. Our results indicate that after menopause, women may need a higher dose of statins or the addition of another lipid-lowering drug. More studies are needed to confirm these findings.”

While young women do have heart attacks, in general, women develop atherosclerosis (narrowing of arteries due to plaque buildup) later in life than men and have heart attacks at an older age than men, in part because of the protective effect of oestrogen. This study examined whether the prognostic importance of atherosclerotic plaques are the same for women and men at different ages as this could be important for selecting treatments to prevent heart attacks.

The study included 24 950 patients referred for coronary computed tomography angiography (CCTA) and enrolled in the CONFIRM registry, which was conducted in six countries in North America, Europe, and Asia. CCTA is used to obtain 3D images of the arteries in the heart.

Total atherosclerotic burden was rated using the Leiden CCTA score, which incorporates the following items for each coronary segment: plaque presence (yes/no), composition (calcified, noncalcified or mixed), location, and severity of narrowing, for a final value of 0 to 42. Patients were divided into three categories previously found to predict the risk myocardial infarction: low atherosclerotic burden (0 to 5), medium (6 to 20) and high (over 20). In addition, obstructive coronary artery disease was defined as 50% narrowing or more.

The primary outcome was the difference in Leiden CCTA score between women and men of similar age. The investigators also analysed sex differences in the rates of major adverse cardiovascular events (MACE), which included all-cause death and myocardial infarction, after adjusting for age and cardiovascular risk factors (hypertension, high cholesterol, diabetes, current smoking and family history of coronary artery disease).

A total of 11 678 women (average age 58.5 years) and 13 272 men (average age 55.6 years) were followed for 3.7 years. Regarding the primary outcome, the study showed an approximately 12 year delay in the onset of coronary atherosclerosis in women: the median Leiden CCTA risk score was above zero at age 64 to 68 years in women versus 52 to 56 years in men (p<0.001). In addition, the overall plaque burden as quantified by the Leiden CCTA score was significantly lower in women, who had more non-obstructive disease.

Dr. van Rosendael said: “The results confirm the previously reported delay in the start of atherosclerosis in women. We also found that women are more likely to have non-obstructive disease. It was formerly thought that only obstructive atherosclerosis caused myocardial infarction but we now know that non-obstructive disease is also risky.”
 
The burden of atherosclerosis was equally predictive of MACE in premenopausal women (aged under 55 years) and men of the same age group. However, in postmenopausal women (age 55 years and older), the risk of MACE was higher than men for a given score. In postmenopausal women, compared to those with a low burden, those with a medium and high burden had 2.21-fold and 6.11-fold higher risks of MACE. While in men aged 55 years and older, compared to those with a low burden, those with a medium and high burden had 1.57-fold and 2.25-fold greater risks of MACE.

Dr van Rosendael said: “In this study, the elevated risk for women versus men was especially observed in postmenopausal women with the highest Leiden CCTA score. This could be partly because the inner diameter of coronary arteries is smaller in women, meaning that the same amount of plaque could have a larger impact on blood flow. Our findings link the known acceleration of atherosclerosis development after menopause with a significant increase in relative risk for women compared to men, despite a similar burden of atherosclerotic disease. This may have implications for the intensity of medical treatment.”

Source: European Society of Cardiology

Categories : Cardiovascular DiseaseTags :

Time to Rethink Beta Blockers as Secondary Prevention for Heart Attack Survivors?

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Secondary prevention after a heart attack, where beta blockers are used over the long term to curb the risk of further heart attacks or death, doesn’t seem to be warranted in patients who don’t have heart failure, suggests a large study published in the journal Heart.

The researchers found no difference in these risks between patients taking beta blockers more than a year after their heart attack and those not on these drugs.

Beta blockers are mostly used to manage abnormal heart rhythms, as well as angina and high blood pressure. They are routinely prescribed after a heart attack as secondary prevention to lower the risk of recurrence and other cardiovascular complications.

But it’s not clear if these drugs are warranted in patients who don’t have heart failure, or a potentially fatal complication of heart attack known as left ventricular systolic dysfunction (LVSD) beyond the first year.

Most of the current evidence is based on the results of clinical trials that predate major changes to the routine care of heart attack patients, explain the researchers.

The researchers drew on 43 618 adults who had had a heart attack between 2005 and 2016 that required hospital treatment, and whose details had been entered into the national Swedish register for coronary heart disease (SWEDEHEART).

None of these patients had heart failure or LVSD: 34 253 of them were prescribed beta blockers and were still on these drugs 1 year after hospital discharge; 9365 hadn’t been prescribed these drugs. Their average age was 64 and around 1 in 4 were women.

The researchers wanted to find out if there were any differences between the two groups in terms of deaths from any cause and rates of further heart attacks, revascularisation, or hospitalisation for heart failure.

The real time data showed that long term treatment with beta blockers wasn’t associated with improved cardiovascular outcomes during an average monitoring period of 4.5 years.

Some 6475 (19%) of those on beta blockers, and 2028 (22%) of those who weren’t, died from any cause, or had another heart attack, or required unscheduled revascularisation, or were admitted to hospital for heart failure.

After accounting for potentially influential factors, including demographics and relevant co-existing conditions, no significant difference was seen in rates of these events between the two groups.

As an observational study, it can’t establish cause. Additionally, despite being the largest study of its kind to date, the findings should be viewed in the context of certain limitations, acknowledge the researchers.

Patients weren’t randomised to treatment; only certain cardiovascular outcomes were included; there was no indication of how consistently patients took their drugs; nor any information on their health related quality of life.

And there were some differences between the two groups in respect of factors known to influence the risk of poor cardiovascular outcomes.

But, the researchers point out, beta blockers are associated with several side effects such as depression and fatigue, and it’s now time to reassess the value of long term treatment with these drugs in heart attack patients who don’t have heart failure or LVSD, they suggest.

In a linked editorial, Professor Ralph Stewart and Dr Tom Evans write: “Despite strong evidence that long-term beta-blockers can improve outcomes after [heart attack], it has been uncertain whether this benefit applies to lower risk patients who are taking other evidence-based therapies and who have a [normal functioning heart].”

They point out: “Recommendations on the duration of beta blocker therapy are variable or absent because this question was not specifically evaluated in clinical trials. Most patients take daily medications for many years after a [heart attack] because they believe they are beneficial.”

And they conclude: “[This] study raises an important question directly relevant to the quality of care –do patients with a normal [functioning heart] benefit from long term beta-blocker therapy after [heart attack]? To answer this question, more evidence from large randomised clinical trials is needed.”

Source: EurekAlert!

Categories : Cardiovascular Disease Medical Industry Metabolic DisordersTags :

Bempedoic Acid Could be a Viable Alternative to Statins

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Bempedoic acid, a new cholesterol-lowering drug, has the potential to be an effective substitute for patients who can’t tolerate statins. Bempedoic acid is an ATP citrate lyase inhibitor that reduces low-density lipoprotein (LDL) cholesterol levels and is associated with a low incidence of muscle-related adverse events. Its effects on cardiovascular outcomes were uncertain, so researchers used a double-blind, randomised, placebo-controlled trial to determine outcomes on a variety of cardiovascular measures in statins-intolerant patients.

The study, published in the New England Journal of Medicine, recruited patients aged 18–85 years at increased cardiovascular risk and unable or unwilling to take statins due to adverse effects. Patients were first tested with placebo over a 4-week run-in period, and were not randomised if they experience unacceptable adverse effects or if adherence was less than 80%. The 13 970 patients who successfully completed run-in were randomised to receive bempedoic acid 180mg orally per day or matching placebo. 

The mean LDL cholesterol level at baseline was 139.0mg/dL in both groups, and after 6 months, the reduction in the level was greater with bempedoic acid than with placebo by 29.2mg/dL; the observed difference in the percent reductions was 21.1 percentage points in favour of bempedoic acid.

Compared to placebo, risk of fatal or nonfatal stroke, death from cardiovascular causes, and death from any cause after significantly were lower by 13%, after a median of 40.6 months of follow-up. The risk of death from cardiovascular causes, nonfatal stroke, or nonfatal myocardial infarction was 15% lower with bempedoic acid than with placebo, and the risks of fatal or nonfatal myocardial infarction and coronary revascularisation were 23% lower and 19% lower, respectively.

The researchers noted that the LDL-cholesterol lowering effects were similar in magnitude and predicted reduction in cardiovascular risks to that observed with statins. In addition, bempedoic acid did not increase glycated haemoglobin levels or the incidence of new-onset diabetes, unlike statins. Due to the demonstrated benefits, those taking placebo were offered the chance to transition to taking bempedoic acid.

A trial limitation was that it only included patients with statins intolerance, and who therefore had higher LDL cholesterol levels at baseline.

Categories : Cardiovascular DiseaseTags :

Iron Drives Chronic Heart Failure in Myocardial Infarction Survivors

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A multi-institution study has found that iron drives the formation of fatty tissue in the heart and leads to chronic heart failure in about 50% of myocardial infarction (MI) survivors. The discovery, recently published in Nature Communications, paves the way for treatments that have the potential to prevent heart failure.

“For the first time, we have identified a root cause of chronic heart failure following a heart attack,” said study leader Rohan Dharmakumar, PhD, of Indiana University School of Medicine.

“While advances across populations have made survival after a heart attack possible for most, too many survivors suffer long-term complications like heart failure,” said Subha Raman, MD, who is physician director of the Cardiovascular Institute. “Dr. Dharmakumar’s breakthrough science illuminates who is at risk and why and points to an effective way to prevent these complications.”

The study followed large animal models over six months. In MI with bleeding complications, scar tissue is slowly replaced by fat. Fatty tissue can’t push blood from the heart effectively, and this is what leads to heart failure and eventually to death in many survivors of haemorrhagic MI, Dharmakumar said.

“Using noninvasive imaging, histology and molecular biology techniques, and various other technologies, we have shown that iron from red blood cells is what drives this process,” he explained. “When we removed the iron, we reduced the amount of fat in the heart muscle. This finding establishes a pathway for clinical investigations to remedy or mitigate the effects associated with iron in haemorrhagic myocardial infarction patients.”

Dharmakumar’s team is currently testing iron chelation therapy to do just that in a just-launched clinical trial.

“Thanks to a clinical trial underway being led by his team at Indiana University, I’m excited to see this treatment improve the lives of millions of heart attack survivors worldwide,” said Raman.

Source: Indiana University School of Medicine

Categories : Cardiovascular Disease Surgeries & ProceduresTags :

Troponin Levels Help Inform When to Perform Surgery after Heart Attack

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New research from a large study published in the International Journal of Cardiology shows that timing of surgery for some heart attack patients can be improved by analysing troponin levels.

Troponin is a protein involved in muscle contraction that is released into the bloodstream after heart attack, with higher levels indicating more heart damage. Troponin levels help clinicians to determine whether a patient is having a heart attack, or myocardial infarction (MI), and to decide on treatment options such as coronary artery bypass graft (CABG) surgery.

The optimal time to perform surgery following an MI remains unclear. Previous reports have suggested that carrying out surgery in the first few days following an MI is associated with a higher risk of surgical complications and death by not leaving time for the heart to recover. As a result, following an MI, many patients who need bypass surgery wait for more than 10 days before surgery is performed.

Researchers in this study found that some patients who have lower levels of troponin would benefit from having earlier surgery. However, the researchers show that patients with very high troponin levels should have surgery postponed, as their risk of dying was higher if surgery was performed within 10 days of their MI.

There was no benefit in delaying surgery for those with low levels of troponin, according to the study.

Early surgery for MI patients

The researchers suggest that early surgery for MI patients with lower troponin levels would reduce overall length of stay and ease pressure on resources such as staff.

This is the first multicentre study to investigate the interaction between the extent of heart damage, as indicated by troponin levels, and the optimal time to wait for surgery in a large series of MI patients. 

Dr Amit Kaura, lead author of the research, said: “The approach on the safest time to operate on patients following a heart attack varies in hospitals across the UK. Our study could help clinicians make more informed decisions on the best treatment plans for heart attack patients requiring surgery, based on their levels of troponin. It could also lead to a more standardised approach in the NHS on how we treat this patient group, leading to resources being used effectively, shorter stays and improved outcomes for patients.”

The study reviewed patients who had a non-ST segment elevation myocardial infarction (NSTEMI) due to a blockage to their coronary arteries who required a CABG.

About 20% of NSTEMI patients have a CABG. The optimal timing for CABG surgery in patients with uncomplicated NSTEMI has been unclear. Prior to the new research, some studies had suggested that early surgery was associated with higher mortality post operation. This has led to a tendency for CABG to be delayed if a patient’s condition remains stable. However, other studies had reported similar mortality rates after early versus late surgery, concluding that delaying surgery in all patients after uncomplicated NSTEMI is not warranted and does not improve outcomes. No previous study had investigated in a large group of patients whether there was an association between the extent of heart damage (as measured by troponin levels) and the wait for surgery on survival.

Heart data insights

The team analysed data from the NIHR HIC of 1746 patients with NSTEMI and unstable angina (UA) where insufficient cardiac blood supply leads to an MI. The cohort consisted of 1684 patients with NSTEMI and 62 with UA. The average age of the group was 69 and 21% were female. They underwent CABG within 90 days at one of five cardiac centres before their surgery between 2010 and 2017. 

The researchers compared patients’ troponin levels, wait between surgery and outcomes after surgery within the first 30 days and over a period of five years. Pre-operative troponin level strongly predicted early mortality, and this was significantly influenced by the interval to surgery. The average wait for patients with high troponin levels to surgery was nine days. Sixty patients died within 30 days after surgery and another 211 patients died over a period of five years following surgery. They found that for those who had troponin levels of less than 100 times the normal upper limit, delaying surgery to after 10 days was not associated with lower survival. For patients with higher troponin levels, early survival increased progressively with a longer time to surgery – survival was highest in those who had surgery after day 10. 

Dr Amit Kaura said: “For patients with troponin levels of under 100 times the normal upper limit, extending the waiting time or surgery did not improve early survival. This finding is particularly significant as two-thirds of patients presenting with troponin levels of under 100 are waiting on average 12 days for surgery after being admitted to hospital. There are potential cost saving implications with our research by performing earlier surgery in this group of patients with lower troponin levels”.

The effect of troponin levels pre-operation on survival was limited to the first 30 days after surgery. Late survival was determined by other risk factors, such as age and other co-morbidities such as hypertension.

Further studies are needed in the form of prospective trials to assess the impact of troponin and timing of surgery on survival following a heart attack, the researchers say.

Source: Imperial College London

Categories : Cardiovascular Disease HIVTags :

People with HIV and Hepatitis C Have Increased Heart Attack Risk

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As people with HIV age, their risk of myocardial infarction increases far more if they also have untreated hepatitis C virus, according to new research published today in the Journal of the American Heart Association.

According to the findings, even with antiretroviral therapy (ART), the risk of myocardial infarction (MI) among people with HIV is at least 50% higher than people without HIV. This new study evaluated if people with HIV who also have hepatitis C have a higher risk of MI.

“HIV and hepatitis C coinfection occurs because they share a transmission route – both viruses may be transmitted through blood-to-blood contact,” said Associate Professor Keri N. Althoff, PhD, MPH, senior author of the study. “Due in part to the inflammation from the chronic immune activation of two viral infections, we hypothesised that people with HIV and hepatitis C would have a higher risk of heart attack as they aged compared to those with HIV alone.”

Researchers analysed health information for 23 361 people with HIV in the North American AIDS Cohort Collaboration on Research and Design (NA-ACCORD) between 2000–2017 started on antiretroviral treatment for HIV, median age 45 at enrolment. One in 5 study participants (4677) were also positive for hepatitis C. During a median follow-up of about 4 years, the researchers compared the occurrence of a heart attack between the HIV-only and the HIV-hepatitis C co-infected groups as a whole, and by each decade of age.

The analysis found:

  • With each decade of increasing age, MI incidence increased 30% in people with HIV alone and 85% in those who were also positive for hepatitis C.
  • The risk of heart attack increased in participants who also had traditional heart disease risk factors such as high blood pressure (more than 3 times), smoking (90%) and Type 2 diabetes (46%).
  • The risk of heart attack was also higher (40%) in participants with certain HIV-related factors such as low levels of CD4 immune cells (200 cells/mm3, signalling greater immune dysfunction) and 45% in those who took protease inhibitors (one type of ART linked to metabolic conditions).

“People who are living with HIV or hepatitis C should ask their doctor about treatment options for the viruses and other ways to reduce their cardiovascular disease risk,” said Assistant Professor Raynell Lang, MD, MSc, lead study author.

“Several mechanisms may be involved in the increased heart attack risk among co-infected patients. One contributing factor may be the inflammation associated with having two chronic viral infections,” A/Prof Lang said. “There also may be differences in risk factors for cardiovascular disease and non-medical factors that influence health among people with HIV and hepatitis C that plays a role in the increased risk.”

“Our findings suggest that HIV and hepatitis C co-infections need more research, which may inform future treatment guidelines and standards of care,” Althoff said.

The study is limited by not having information on additional factors associated with heart attack risk such as diet, exercise or family history of chronic health conditions. Results from this study of people with HIV receiving care in North America may not be generalizable to people with HIV elsewhere. In addition, the study period included time prior to the availability of more advanced hepatitis C treatments.

“Because effective and well-tolerated hepatitis C therapy was not available during several years of our study period, we were unable to evaluate the association of treated hepatitis C infection on cardiovascular risk among people with HIV. This will be an important question to answer in future studies,” Lang said.

Source: American Heart Association

Categories : Cardiovascular DiseaseTags :

Gout Flare-ups Linked to Increased MI and Stroke Risk

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The risk of myocardial infarction (MI) and strokes temporarily increases in the four months after a gout flare, suggests a study published in the journal JAMA.

The findings showed that gout patients who suffered from an MI or stroke were twice as likely to have had a gout flare in the 60 days prior to the event, and one and a half times more likely to have a gout flare in the 61-120 days prior.

Gout is a common form of arthritis that is caused by high levels of uric acid, a chemical produced by breakdown of body tissues and present in certain foods and drinks.

At high levels, uric acid is deposited in and around joints as needle shaped urate crystals. Once released from their deposits, these crystals cause severe inflammation that manifest as joint pain, swelling, redness, and tenderness that often lasts for 1–2 weeks. These episodes, called gout flares, often recur. Inflammation is also a risk factor for heart attack and stroke.

While gout patients tend to have more cardiovascular risk factors, there have been no previous studies about whether gout flares are linked with an increased risk of MI and stroke.

To address this, the team used data from 62 574 patients with gout treated in the NHS. Of these, 10 475 experienced heart attack or stroke after the diagnosis of gout, while matched controls did not experience such events. They evaluated the association between heart attacks or strokes and recent gout flares and adjusted these results for possible confounding factors. They found that gout patients who suffered an MI or stroke were twice as likely to have had a gout flare in the 60 days prior to the event, and one and a half times more likely to have a gout flare in the preceding 61–120 days.

They found a similar high rate of MI or stroke in the 0–60 and 61–120 days after gout flares compared with other time periods, when they used information from only patients who consulted for a gout flare and also experienced either MI or stroke. This further strengthened the finding that gout flares are associated with a transient increase in cardiovascular events following flares. The increased odds and rates persisted when people with pre-existing heart disease or stroke before their gout diagnosis were excluded, and when shorter exposure periods such as 0-15 and 16-30 days prior to MI or stroke, were considered.

Gout patients who died from a MI or stroke had over four times the odds of experiencing a gout flare in the preceding 0-60 days and over twice the odds of gout flare in the preceding 61-120 days.

The study’s lead author, Professor Abhishek at the University of Nottingham, said: “This is the first study of its kind to examine whether there is an association between recent gout flares and heart attacks and strokes.

“The results show that among patients with gout, patients who experienced a heart attack or stroke had significantly increased odds of a gout flare during the preceding 120-days compared with patients who did not experience such events. These findings suggest that gout flares are associated with a transient increase in cardiovascular events following flares.

“People with recurrent gout flares should be considered for long-term treatment with urate lowering treatments such as allopurinol. This is a reliable way of removing urate crystal deposits and providing freedom from gout flares. Patients should also be considered for concurrent treatment with anti-inflammatory medicines such as colchicine for the first few months because urate lowering treatments may trigger gout flares in the short term.

“People with gout should be encouraged to adopt a healthy lifestyle with appropriate treatment of conditions such as high blood pressure, high cholesterol, obesity and diabetes to minimise their background risk of heart attack and stroke.”

Source: University of Nottingham

Categories : Cardiovascular DiseaseTags :

Beta Blockers and Antiplatelet Drugs Tied to Heat-related MI Risk

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During hot weather events, people taking beta blockers and antiplatelet medications such as aspirin could be at increased risk of a myocardial infarction (MI), amplifying the risk already present from hot weather.

A new study published in Nature Cardiovascular Research found that, among people suffering non-fatal MI associated with hot weather, a greater portion are taking these heart drugs.

“Patients taking these two medications have higher risk,” said Assistant Professor Kai Chen, first author of the study. “During heat waves, they should really take precautions.”

External environmental factors like air pollution and cold weather can trigger MIs, and there is growing evidence to suggest that hot weather can do so, too. But epidemiologists are still working to identify which groups of people are most vulnerable to these environmental extremes.

The authors looked at 2494 cases sourced from a registry, in which individuals experienced a non-fatal MI in Augsburg, Germany during the hot-weather months (May–September) between 2001 and 2014.

In previous research, they had shown that exposure to either heat or cold made heart attacks more likely, and they calculated that heat-related MI rates would rise once the planet has warmed by 2–3°C.

The current study built on that research by examining patients’ medication use prior to their MI.

They analysed the data in a way that let patients serve as their own controls, by comparing heat exposure on the day of the MI versus the same days of the week within the same month. That is, if a person had an NI on the third Thursday in June, the authors compared their temperature exposure that day to their temperature exposure on other, “control” Thursdays in June.

It turned out that users of beta-blockers or antiplatelet medications were likelier to have an MI during the hottest days compared to control days. Antiplatelet medication use was associated with a 63% increase in risk and beta-blockers with a 65% increase. People taking both drugs had a 75% higher risk. Non-users of those medications were not more likely to have a heart attack on hot days.

When researchers compared younger patients (25–59 years) to older ones (60–74 years), they found, as expected, that the younger ones were a healthier group, with lower rates of coronary heart disease. Yet younger patients taking beta-blockers and antiplatelet medications were more susceptible to heat-related heart attack than older patients, despite the older ones having more heart disease.

Another clue that these two medication types may render people more vulnerable is that, other heart medications generally didn’t show a connection to heat-related heart attacks. An exception was statins, which taken by younger people, were associated with an over threefold risk of a heart attack on hot days.

“We hypothesise that some of the medications may make it hard to regulate body temperature,” Asst Prof Chen said. He plans to find out why in future studies.

The results suggest that as climate change progresses, heart attacks might become a greater hazard to some people with cardiovascular disease.

Source: Yale School of Public Health

Categories : Cardiovascular DiseaseTags :

Study Sheds Light on Cardiac Repair after MI

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Photo from Olivier Collett on Unsplash

Immune response and the lymphatic system are central to cardiac repair after a heart attack, according to a study published in the Journal of Clinical Investigation. These insights into the basic mechanisms of cardiac repair pave the way towards the development of new treatments to preserve heart function.

“We found that macrophages, or immune cells that rush to the heart after a heart attack to ‘eat’ damaged or dead tissue, also induce vascular endothelial growth factor C (VEGFC) that triggers the formation of new lymphatic vessels and promotes healing,” said co-senior author Edward Thorp, PhD, from the Heart Center at Lurie Children’s and Associate Professor of Pathology and Pediatrics at Northwestern University Feinberg School of Medicine. “Our challenge now is to find a way either to administer VEGFC or to coax these macrophages to induce more VEGFC, in order to speed the heart repair process.”

People who suffer a heart attack are at high risk for heart failure, even with the advances in medications to reduce mortality. This occurs in part because some macrophages that arrive at the site of damage are proinflammatory and do not induce VEGFC.

“It is a Dr. Jekyll and Mr. Hyde scenario, with ‘good’ macrophages that induce VEGFC and the ‘bad’ ones that don’t. We need to prevent the ‘bad’ macrophages from causing further damage,” said co-senior author Guillermo Oliver, PhD, Director of Feinberg Cardiovascular and Renal Research Institute – Center for Vascular and Developmental Biology, and Professor of Medicine at Northwestern University Feinberg School of Medicine. “We are working to understand more about the progression to heart failure after a heart attack, in order to intervene early and reset the course to cardiac repair.”

Source: DICardiology

Categories : Cardiovascular DiseaseTags :

Thoracic Aorta Diameter Can Predict Cardiovascular Risk

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Anatomical model of a human heart
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A new study in the journal Radiology has found that the diameter of the thoracic aorta can be a biomarker for heart attacks and other adverse cardiovascular events in women and men, and has the advantage of being simple to add on to existing screening.

The thoracic aorta is divided into an ascending aorta that rises from the left ventricle of the heart and a descending aorta in the back of the chest.

While the thoracic aorta grows with age, but changes of vessel size and structure, a phenomenon known as vascular remodelling, have a systemic nature involving haemodynamic and biological processes that are also linked to cardiovascular disease.

“While enlargement of the thoracic aorta is a frequent finding in clinical practice, few longitudinal data regarding its long-term prognosis for major cardiovascular disease outcomes at the population level exist,” said study senior author Maryam Kavousi MD, PhD, from University Medical Center Rotterdam.

Dr Kavousi and colleagues assessed these associations in 2178 participants from the population-based Rotterdam Study. Participants underwent multi-detector CT scans between 2003 and 2006 and were followed for an average of 9 years. Thoracic aorta diameters were indexed for body mass index (BMI).

Larger BMI-indexed ascending and descending thoracic aortic diameters were significantly associated with increased risk of adverse cardiovascular outcomes like stroke and death in both women and men.

“Our results suggest that imaging-based assessment of diameter of thoracic aorta can be considered as a risk marker for future cardiovascular disease,” Dr Kavousi said.

In women, greater ascending aortic diameter was associated with 33% higher cardiovascular mortality risk. There seems to be a sex difference in remodelling of the ageing aorta, with faster deterioration in women.

“Ageing could affect aortic health and structure more adversely in women than in men,” Dr Kavousi said.

The study findings suggest that cardiovascular risk assessment associated with thoracic aortic size among asymptomatic women and men could lead to effective, sex-specific prevention strategies.

“As the aortic diameter is significantly related to body size, use of aortic diameters indexed for body measurements could improve its prognostic value for cardiovascular outcomes,” Dr Kavousi said.

Measurement of thoracic aorta size is an easy addition to current screening, the researchers said. The study made use of cardiac CT scans that are already commonly used to assess coronary calcium. Thoracic aortic diameter could also be measured routinely, for example as part of CT-based lung cancer screening.

The current study was based on a single CT-based assessment of thoracic aorta among a large group of participants from the general population, followed up for nine years for incidence of cardiovascular outcomes and mortality. The researchers have recently repeated the CT-based assessment of thoracic aorta among these participants after a median of 14 years.

“This provides an exciting and unique opportunity to study sex-specific risk profiles and patterns of growth in thoracic aorta in the general population,” Dr Kavousi said.

Source: Radiological Society of North America