Findings from new research published in Diabetes, Obesity and Metablismsuggest that people with type 2 diabetes may need to reduce their blood sugar levels sooner after diagnosis than previously thought, to prevent major cardiovascular events such as heart attacks.
The University of Surrey study Surrey suggests that achieving glycaemic control within the first year of diagnosis reduces the incidence of major cardiovascular events. Additionally, the team found that the greater the variation in blood levels 12-months after diagnosis, the more likely a patient was to experience dangerous cardiovascular events.
Dr Martin Whyte, co-author of the study and Reader in Metabolic Medicine at the University of Surrey, said: “The conventional wisdom has been to slowly and steadily treat type 2 diabetes with diet and medicine dose-escalation over years – the period over which it took people to reduce their sugar levels after diagnosis was thought less important for major vascular protection. However, our observational study suggests that getting blood levels under control quickly — within the first 12 months after diagnosis — will significantly help reduce cardiovascular events.”
Type 2 diabetes is a common condition that results in the level of sugar in the blood becoming too high. The condition is linked to obesity or a family history of type 2 diabetes and can increase a person’s risk of getting serious health conditions.
The University of Surrey’s study used Royal College of General Practitioners’ Research and Surveillance Centre database to perform a comprehensive examination of glycaemic control achieved within the first year of diagnosis and subsequent blood sugar level variability with cardiovascular disease incidents.
Vascular endothelial cells use a vast network of connections to control all cardiovascular functions and the risk of developing cardiovascular disease, according to a new study published in PNAS.
It has long been known that the development of these conditions begins with changes in the vascular endothelial cells lining the body’s blood vessels. But why and how changes in endothelial cell function occur is not entirely clear.
Research has revealed that these cells communicate with each other using a sophisticated system. Failures in this communication system may be the first step in the development of cardiovascular disease.
The endothelium, which forms the thin inner layer of cells in blood vessels, regulates blood flow, blood pressure, blood clotting, inflammation and response to disease. On a continual basis, it processes the vast amounts of information held in the composition of blood, and chemicals in the area around each blood vessel to keep the cardiovascular system working properly.
The study identified clusters of cells in the endothelium that are specialised to particular functions and they operate in ‘cliques’. Between cliques, numerous interlinked connections act to convey information, with a high density of connections to protect the system against communication failures. The system bypasses neighbouring cells by use of shortcuts to transmit information quickly over distance.
The endothelial communication network design is in fact remarkably similar to the communication operations of the internet and it is effective for local blood vessel control and global efficiency in determining overall cardiovascular activity. The design is robust, so that communication systems to control cardiovascular activity will not fail even when there is extensive damage.
The findings also indicate that changes in the organisation of communication, rather than behaviour and function of individual cells, may underlie disease.
The researchers addressed the nature of the communication network by using single-cell calcium ion imaging across thousands of endothelial cells in intact blood vessels and applying mathematical network (graph) theory.
Professor John McCarron at Strathclude University said: “Cells in the endothelium are a major target for the control of cardiovascular disease and are often treated as being a uniform population of cells. Our findings show the cells are not uniform but specialised to particular types of function.
“There is a well-organised, rapid and robust communication system that shares information so that co-ordinated responses occur. The communication system offers new targets for therapy development and insights into why developing treatments has proven so difficult.”
The US Preventive Services Task Force (USPSTF) has issued a recommendation statement on the use of aspirin in the prevention of cardiovascular disease (CVD). The recommendation shifts the use of aspirin to an earlier window, and making it an individualised decision for people in their 40s to 50s with a > 10% 10-year CVD risk.
The previous recommendation from 2016had called for low-dose aspirin for people in their 50s with a > 10% 10-year CVD risk and individualised decisions for those in their 60s with similar risk. The update comes after new evidence emergedin a number of randomised controlled trials.
For the update, which appears in JAMA Network, a systematic review was conducted on the effectiveness of aspirin to reduce the risk of CVD events (myocardial infarction and stroke), cardiovascular mortality, and all-cause mortality in persons without a history of CVD. The effect of aspirin use on colorectal cancer incidence and mortality was also investigated in primary CVD prevention populations, as well as the harms (particularly bleeding) associated with aspirin use.
The USPSTF concludes with moderate certainty that aspirin use for the primary prevention of CVD events in adults aged 40–59 years with a 10% or greater 10-year CVD risk has a small net benefit, and starting low-dose aspirin use for CVD prevention should be an individual decision for them. Those not at increased risk for bleeding and are willing to take low-dose aspirin daily are more likely to benefit. The USPSTF recommends against initiating low-dose aspirin use for the primary prevention of CVD in adults 60 years or older.
Aspirin’s mechanism of action in CVD protection is well known. Aspirin at low doses is an irreversible cyclooxygenase 1 (COX-1) enzyme inhibitor, and at higher doses, it also inhibits COX-2. By inhibiting platelet function through COX-1, aspirin reduces atherothrombosis risk, and has been used widely for the prevention of CVD events, particularly for secondary prevention. However the COX-1 is also involved with protection of the gastrointestinal mucosa, and inhibition of it can promote gastrointestinal bleeding. The mechanism for the possible antineoplastic effects of aspirin is not as well understood.
Older age is one of the strongest risk factors for CVD, and men have a higher overall CVD disease burden and tend to experience CVD events earlier in life. Race and ethnicity affects CVD burden, with Black persons having the highest prevalence of CVD.
Similar CVD benefits appear for a low aspirin dose (≤ 100mg/d) and for all doses that have been studied in CVD prevention trials (50 to 500mg/d). A pragmatic approach would be to use 81 mg/d, which is the most commonly prescribed dose in the US.
Because CVD risk estimation is imprecise and imperfect at the individual level, the USPSTF suggests using these risk estimates as a starting point to discuss with appropriate candidates their desire for daily aspirin use. The benefits of initiating aspirin use are greater for individuals at higher risk for CVD events (eg, those with > 15% or > 20% 10-year CVD risk).
In addition to age and estimated level of CVD risk, decisions about initiating aspirin use should be based on shared decision-making between clinicians and patients about the potential benefits and harms, based on the relative values the patient places on these (reduced CVD risk vs increased bleeding and stroke risk).
Annual bleeding events in individuals without risk factors for increased bleeding (eg, history of gastrointestinal bleeding risk, history of peptic ulcer disease, or use of nonsteroidal anti-inflammatory drugs or corticosteroids) are rare, but risk for bleeding increases modestly with advancing age. For persons who have initiated aspirin use, the net benefits continue to accrue over time in the absence of a bleeding event. However, benefits shrink with advancing age because of increased bleeding risk, with modelling data suggesting stopping aspirin use around age 75.
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.
A study published in JAMA Network Open showed that cereal fibre but not fruit or vegetable fibre, was consistently associated with lower inflammation and lower CVD incidence. Until now there had been limited data on the link between fiber and inflammation among older adults, who have higher levels of inflammation compared with younger adults.
The research includes data from a large and well-characterised prospective cohort of elderly individuals, with detailed data on dietary intake, inflammation, and incidence of CVD. The research confirmed previously observed associations between dietary fibre and CVD and extended those investigations to include the source of the fibre, the relationship of fibre with multiple inflammatory markers, and to test whether inflammation mediated the relationship between dietary fibre and CVD.
Of the 4125 adults enrolled in the Cardiovascular Health Study from 1989 to 1990 participants received a food frequency questionnaire that was administered to those without prevalent CVD at enrollment and then were followed up visits for development CVD (stroke, myocardial infarction, and atherosclerotic cardiovascular death) through June 2015. Blood samples were assessed for markers of inflammation.
“Higher intakes of dietary fiber is associated with lower CVD risk. A common hypothesis has been that higher fiber intakes reduce inflammation, subsequently leading to lower CVD risk,” said Rupak Shivakoti, PhD. ‘With findings from this study, we are now learning that one particular type of dietary fiber — cereal fibre — but not fruit or vegetable fibre was associated with lower inflammation. With findings from this study we now are learning that cereal fiber has the potential to reduce inflammation and will need to be tested in future interventional studies.”
Although there are data to suggest that fibre in general might have anti-inflammatory effects by improving gut function, modifying diet and satiety (eg, reduced fat and total energy intake), and improving lipid and glucose profile metabolism, why cereal fibre but not vegetable or fruit fibre is associated with lower inflammation is not clear and warrants further investigation, noted Dr Shivakoti. Additionally, it is unclear whether it is the cereal fibre itself or other nutrients in foods rich in cereal fibre behind the observed relationships.
“Additionally, we learned that inflammation had only a modest role in mediating the observed inverse association between cereal fiber and CVD,” observed Dr Shivakoti. “This suggests that factors other than inflammation may play a larger role in the cereal fiber-associated reduction in CVD and will need to be tested in future interventions of specific populations.
By tracking more than 38 000 participants from childhood for fifty years, researchers have uncovered direct evidence that the five cardiovascular risk factors when present in childhood predicted cardiovascular risk in adulthood.
Body mass index, blood pressure, cholesterol, triglycerides and youth smoking, particularly in combination in early childhood, were clinically linked with cardiovascular events that predict poor cardiovascular health in adults.
Paper co-author Prof Terence Dwyer at the University of Oxford commented: “Despite the effect medical and surgical care have had on treating heart disease, achieving the greatest possible reduction in the heart disease burden will depend on including preventive strategies that commence in childhood.”
The findings confirm that prevention must start in childhood. “Longitudinal studies like these have been hampered by a lack of inclusion of comprehensive childhood data around body measurements, blood pressure, and blood lipids and a failure to follow-up at ages when cardiovascular disease becomes common.”
The study involved 38 589 participants from Australia, Finland and the US, who were followed from age 3-19 years for a period of 35-50 years.
The results showed that increased risk for cardiovascular events was seen in over half the children, with those having the highest risk factor levels, at 9 times the risk for an event as for children with below average risk factors.
“While this evidence had not been available previously, the findings were not entirely surprising as it had been known for some time that children as young as five already showed early signs of fatty deposits in arteries. This new evidence justified a greater emphasis on programs to prevent the development of these risk factors in children. Clinicians and public health professionals should now start to focus on how this might best be achieved,” Prof Dwyer concluded.
Findings from a new show that an experimental ‘gene silencing’ therapy reduced blood levels of lipoprotein(a) by up 98%. This is significant as lipoprotein(a) is a key cardiovascular risk driver which is determined largely by genetics and not modifiable lifestyle factors, and which cannot be lowered by current medical means.
Trial participants receiving higher doses of SLN360 – a small interfering RNA (siRNA) therapeutic that ‘silences’ the gene responsible for lipoprotein(a) production – saw their lipoprotein(a) levels drop by as much as 96%-98%. Five months later, these participants’ lipoprotein(a) – also known as Lp(a) – levels remained 71%-81% lower than baseline.
The findings suggest this siRNA therapy could be a promising treatment to help prevent premature heart disease in people with high levels of Lp(a), which is estimated to affect 64 million people in the United States and 1.4 billion people worldwide.
“These results showed the safety and strong efficacy of this experimental treatment at reducing levels of Lp(a), a common, but previously untreatable, genetically-determined risk factor that leads to premature heart attack, stroke and aortic stenosis,” said the study’s lead author Steven E. Nissen, MD “We hope that further development of this therapy also will be shown to reduce the consequences of Lp(a) in the clinical setting through future studies.”
Lp(a) has similarities to LDL. Lp(a) is made in the liver, where an extra protein called apolipoprotein(a) is attached to an LDL-like particle. Unlike other types of cholesterol particles, Lp(a) levels are 80 to 90% genetically determined. The structure of the Lp(a) particle causes the accumulation of plaques in arteries, which play a significant role in heart disease. Elevated Lp(a) greatly increases the risk of heart attacks and strokes.
Although cardiovascular risk-reduction therapies that lower LDL cholesterol and other lipids exist, there are treatments to lower Lp(a). Since Lp(a) levels are genetically determined, lifestyle changes such as diet or exercise have no effect. In the current study, the siRNA therapy reduces Lp(a) levels by “silencing” the gene responsible for Lp(a) production and blocking creation of apolipoprotein(a) in the liver.
In the APOLLO trial, researchers enrolled 32 participants with Lp(a) levels above 15 nmol/L, with a median level of 224nmol/L (75nmol/L or less is considered normal). Eight participants received a placebo and the remaining received one of four doses of SLN360 via a single subcutaneous injection. The doses were 30mg, 100mg, 300mg and 600mg. Participants were closely observed for the first 24 hours after their injection and then followed up for five months.
Compared to baseline, participants receiving 300mg and 600mg of SLN360 experienced a maximum of 96% and 98% reduction in Lp(a) levels, and a reduction of 71% and 81% at five months. Those receiving a placebo saw no change in Lp(a) levels. The highest doses also reduced LDL cholesterol by about 20%-25%. There were no major safety consequences reported and the most common side effect was temporary soreness at the injection site. The study was extended and researchers will continue to follow participants for a total of one year.
Though light alcohol consumption may provide heart-related health benefits has been suggested observational research, a large study published in JAMA Network Open showed a link between all levels of alcohol intake and higher risks of cardiovascular disease. The researchers found that the supposed benefits of alcohol consumption may in fact be attributable to other healthy lifestyle factors common among light to moderate drinkers.
The study included 371 463 adult participants from the UK Biobank, average age 57 and consuming an average of 9.2 drinks per week. In line with previous findings, researchers found that the lowest heart disease risk was in light to moderate drinkers, followed by people who abstained from drinking. People who drank heavily had the highest risk. However, light to moderate drinkers also tended to have healthier lifestyles than abstainers, such as more physical activity and vegetable intake, and less smoking. One a few lifestyle factors were taken into account, any benefit associated with alcohol consumption was significantly reduced.
The study also used new techniques in Mendelian randomisation, which uses genetic variants to determine whether an observed link between an exposure and an outcome is consistent with a causal effect. “Newer and more advanced techniques in ‘non-linear Mendelian randomisation’ now permit the use of human genetic data to evaluate the direction and magnitude of disease risk associated with different levels of an exposure,” said senior author Krishna G. Aragam, MD, MS, a cardiologist at MGH and an associate scientist at the Broad Institute. “We therefore leveraged these new techniques and expansive genetic and phenotypic data from biobank populations to better understand the association between habitual alcohol intake and cardiovascular disease.”
When such genetic analyses were performed on samples taken from participants, they found that individuals with genetic variants that predicted higher alcohol consumption were indeed more likely to consume greater amounts of alcohol, and more likely to have hypertension and coronary artery disease. The analyses also revealed significant differences in cardiovascular risk across the spectrum of alcohol consumption for both males and females, with minimal risk increase when going from zero to seven drinks per week, much higher risk increases when progressing from seven to 14 drinks per week, and greatly increased risk for 21 or more drinks per week. Notably, the findings suggest a rise in cardiovascular risk even at “low risk” levels (ie below two drinks per day for men and one per day for women).
This discovery of an exponential rather than liner relationship between alcohol intake and cardiovascular risk is was supported by an additional analysis of data on 30 716 participants in the Mass General Brigham Biobank. Therefore, cutting back on large consumption of alcohol may have even more clinical benefits than cutting back on moderate amounts.
“The findings affirm that alcohol intake should not be recommended to improve cardiovascular health; rather, that reducing alcohol intake will likely reduce cardiovascular risk in all individuals, albeit to different extents based on one’s current level of consumption,” said Dr Aragam.
The American College of Cardiology has issued an expert consensus decision pathway for the evaluation and management of adults with key cardiovascular consequences of COVID. The document discusses myocarditis and other types of myocardial involvement, patient-centred approaches for long COVID and guidance on resumption of exercise following COVID. The clinical guidance was published today in the Journal of the American College of Cardiology.
“The best means to diagnose and treat myocarditis and long COVID following SARS-CoV-2 infection continues to evolve,” said Ty Gluckman, MD, MHA, co-chair of the expert consensus decision pathway. “This document attempts to provide key recommendations for how to evaluate and manage adults with these conditions, including guidance for safe return to play for both competitive and non-competitive athletes.”
Myocarditis is a condition defined by the presence of cardiac symptoms such as chest pain, an elevated cardiac troponin, and abnormal ECG, cardiac imaging and/or cardiac biopsy findings.
Although rare, myocarditis with COVID is more commonly seen in men, and since it is associated with a higher risk of cardiac complications, a proactive management plan should be in place. For mild or moderate myocarditis, hospitalisation is recommended to closely monitor for worsening symptoms, while undergoing follow-up testing and treatment. Patients with severe myocarditis should ideally be hospitalised at appropriately equipped centres.
Myocarditis following COVID-19 mRNA vaccination is also rare and the benefits outweigh the risks. It is most commonly seen in younger males (40.6 cases per million for ages 12–29). Although most cases of myocarditis following COVID mRNA vaccination are mild, it should be diagnosed and treated similarly to myocarditis following COVID infection.
Post-acute sequelae of SARS-CoV-2 infection (PASC), or long COVID, is reported by up to 10-30% of infected individuals. It is defined by a constellation of new, returning or persistent health problems experienced by individuals four or more weeks after COVID infection. While individuals with this condition may experience wide-ranging symptoms, tachycardia, exercise intolerance, chest pain and shortness of breath represent some of the symptoms that draw increased attention to the cardiovascular system.
The writing committee has proposed two terms to better understand potential aetiologies for those with cardiovascular symptoms:
PASC-CVD, or PASC-Cardiovascular Disease, refers to a broad group of cardiovascular conditions (including myocarditis) that manifest at least four weeks after COVID infection.
PASC-CVS, or PASC-Cardiovascular Syndrome, includes a wide range of cardiovascular symptoms without objective evidence of cardiovascular disease following standard diagnostic testing.
Generally, patients with long COVID and cardiovascular symptoms should undergo evaluation with laboratory tests, ECG, echocardiogram, ambulatory rhythm monitor and/or additional pulmonary testing based on the clinical presentation. Cardiology consultation is recommended for abnormal test results, with additional evaluation based on the suspected clinical condition (eg, myocarditis).
Because multiple factors likely underlie PASC-CVS, evaluation and management may be best driven by the predominant cardiovascular symptom(s). For those with tachycardia and exercise intolerance, increased bedrest and/or a decline in physical activity may trigger cardiovascular deconditioning with progressive worsening of symptoms.
“There appears to be a ‘downward spiral’ for long COVID patients. Fatigue and decreased exercise capacity lead to diminished activity and bedrest, in turn leading to worsening symptoms and decreased quality of life,” said Nicole Bhave, MD, co-chair of the expert consensus decision pathway. “The writing committee recommends a basic cardiopulmonary evaluation performed upfront to determine if further specialty care and formalized medical therapy is needed for these patients.”
For PASC-CVS patients with tachycardia and exercise intolerance, upright exercise (walking or jogging) should be replaced with recumbent or semi-recumbent exercise (rowing, swimming or cycling) to avoid worsening fatigue. Exercise intensity and duration should be low initially, with gradual increases in exercise duration over time. Transition back to upright exercise can be done as symptoms improve. Additional interventions (increased salt and fluid intake, elevation of the head during sleep, support stockings) and pharmacological treatments (beta-blockers) should be considered on a case-by-case basis.
Return to Play
Concerns arose about return to play for athletes after COVID due to observations of cardiac injury among some hospitalised COVID patients, along with uncertainty around cardiovascular sequelae after mild illness. However, data do not show a low prevalence of clinical myocarditis and no increase of cardiac events.
For athletes recovering from COVID with ongoing cardiopulmonary symptoms or those requiring hospitalisation with increased suspicion for cardiac involvement, further evaluation with triad testing (ECG, cardiac troponin and echocardiogram) should be performed. For those with abnormal test results, further evaluation with cardiac MRI should be considered. Individuals diagnosed with clinical myocarditis should abstain from exercise for three to six months.
Cardiac testing is not recommended for asymptomatic individuals following COVID infection. Individuals should abstain from training for three days to ensure that symptoms do not develop. For those with mild or moderate non-cardiopulmonary symptoms (fever, lethargy, muscle aches), training may resume after symptom resolution. For those with remote infection (≥ three months) without ongoing cardiopulmonary symptoms, a gradual increase in exercise is recommended without the need for cardiac testing.
Based on the low prevalence of myocarditis observed in competitive athletes with COVID-19, the authors note that these recommendations can be reasonably applied to high-school athletes (aged ≥ 14 years) along with adult recreational exercise enthusiasts. Future study is needed, however, to better understand how long cardiac abnormalities persist following COVID infection and the role of exercise training in long COVID.
Among young and middle-aged adults with high blood pressure, a substantial rise in blood pressure upon standing may identify those with a higher risk of serious cardiovascular events, such as heart attack and stroke, according to new research published in the journal Hypertension.
“This finding may warrant starting blood-pressure-lowering treatment including medicines earlier in patients with exaggerated blood pressure response to standing,” said Professor Paolo Palatini, MD, lead author of the study.
Blood pressure usually falls slightly upon standing up. In this study, researchers assessed whether the opposite response – a significant rise in systolic blood pressure upon standing – is a risk factor for heart attack and other serious cardiovascular events.
Researchers recruited 1207 people aged 18-45 years old with untreated stage 1 hypertension, from the ongoing HARVEST study which started in 1990. Stage 1 hypertension was defined as systolic blood pressure of 140–159 mm Hg and/or diastolic BP 90–100 mm Hg. None had taken blood pressure-lowering medication prior to the study, and all were initially classed as low risk for major cardiovascular events based on lifestyle and medical history.
The researchers took six blood pressure measurements in various physical positions, including when lying down and after standing up. The 120 participants with the highest rise (top 10%) in blood pressure upon standing averaged an 11.4mmHg increase; all increases in this group were greater than 6.5mmHg. Remaining participants averaged a 3.8mmHg fall in systolic blood pressure upon standing.
The researchers compared heart disease risk factors, laboratory measures and the occurrence of major cardiovascular events (heart attack, heart-related chest pain, stroke, aneurysm of the aortic artery, clogged peripheral arteries) and chronic kidney disease among participants in the two groups. In some analyses, the development of atrial fibrillation, an arrhythmia that is a major risk factor for stroke, was also noted. Results were adjusted for age, gender, parental history of heart disease, and several lifestyle factors and measurements taken during study enrolment.
During an average 17-year follow-up, there were 105 major cardiovascular events among the participants. The most common were heart attack, heart-related chest pain and stroke.
People in the top 10% for rise in blood pressure:
had nearly twice the risk for a major cardiovascular event compared to the others;
did not generally have a higher risk profile for cardiovascular events during their initial evaluation (outside of the exaggerated blood pressure response to standing);
were more likely to be smokers (32.1% vs 19.9% in the non-rising group), yet physical activity levels were comparable, and they were not more likely to be overweight or obese, and no more likely to have a family history of cardiovascular events;
had more favourable cholesterol levels (lower total cholesterol and higher high-density-lipoprotein cholesterol);
had lower systolic blood pressure when lying down than the other group (140.5 mm Hg vs. 146.0 mm Hg, respectively), yet blood pressure measures were higher when taken over 24 hours.
After adjusting for average blood pressure taken over 24 hours, an exaggerated blood pressure response to standing remained an independent predictor of adverse heart events or stroke.
“The results of the study confirmed our initial hypothesis – a pronounced increase in blood pressure from lying to standing could be prognostically important in young people with high blood pressure. We were rather surprised that even a relatively small increase in standing blood pressure (6-7 mm Hg) was predictive of major cardiac events in the long run,” said Prof Palatini.
In a subset who had stress hormones measured from 24-hour urine samples, the epinephrine/creatinine ratio was higher in the people with rising BP compared to non-risers (118.4 nmol/mol vs 77.0 nmol/mol, respectively).
“Epinephrine levels are an estimate of the global effect of stressful stimuli over the 24 hours. This suggests that those with the highest blood pressure when standing may have an increased sympathetic response to stressors,” said Prof Palatini. “Overall, this causes an increase in average blood pressure.”
“The findings suggest that blood pressure upon standing should be measured in order to tailor treatment for patients with high blood pressure, and potentially, a more aggressive approach to lifestyle changes and blood-pressure-lowering therapy may be considered for people with an elevated blood pressure response to standing,” he said.