Category: Cardiovascular Disease

Categories : Cardiovascular DiseaseTags :

Signalling Control Explains Why Adult Hearts Cells Don’t Regenerate

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New research published in Developmental Cell has uncovered a possible explanation for why explain why adult heart cells lack regeneration capacity. As heart cells mature in mice, the number of communication pathways called nuclear pores dramatically decreases. While this might protect the organ from damaging signals, it could also prevent adult heart cells from regenerating, the researchers found.

The study, from University of Pittsburgh and UPMC scientists, suggests that quieting communication between heart cells and their environment protects this organ from harmful signals related to stresses such as high blood pressure, but at the cost of preventing heart cells from receiving signals that promote regeneration.

“This paper provides an explanation for why adult hearts do not regenerate themselves, but newborn mice and human hearts do,” said senior author Bernhard Kühn, MD, professor of paediatrics. “These findings are an important advance in fundamental understanding of how the heart develops with age and how it has evolved to cope with stress.”

While skin and many other tissues of the human body retain the ability to repair themselves after injury, the same isn’t true of the heart. During human embryonic and foetal development, heart cells undergo cell division to form the heart muscle. But as heart cells mature in adulthood, they enter a terminal state in which they can no longer divide.

To understand more about how and why heart cells change with age, Prof Kühn teamed up with fellow Pitt researchers to look at nuclear pores. These perforations in the lipid membrane that surround a cell’s DNA regulate the passage of molecules to and from the nucleus.

“The nuclear envelope is an impermeable layer that protects the nucleus like asphalt on a highway,” said Prof Kühn. “Like manholes in this asphalt, nuclear pores are pathways that allow information to get through the barrier and into the nucleus.”

Using super-resolution microscopy, the researchers visualised and counted the number of nuclear pores in mouse heart cells, or cardiomyocytes. The number of pores decreased by 63% across development, from an average of 1,856 in foetal cells to 1040 in infant cells to just 678 in adult cells. These findings were validated with electron microscopy to show that nuclear pore density decreased across heart cell development.

In previous research, Prof Kühn and his team showed that a gene called Lamin b2, which is highly expressed in newborn mice but declines with age, is important for cardiomyocyte regeneration.

In the new study, they show that blocking expression of Lamin b2 in mice led to a decrease in nuclear pore numbers. Mice with fewer nuclear pores had diminished transport of signalling proteins to the nucleus and decreased gene expression, suggesting that reduced communication with age may drive a decrease in cardiomyocyte regenerative capacity.

“These findings demonstrate that the number of nuclear pores controls information flux into the nucleus,” explained Prof Kühn. “As heart cells mature and the nuclear pores decrease, less information is getting to the nucleus.”

In response to stress such as high blood pressure, a cardiomyocyte’s nucleus receives signals that modify gene pathways, leading to structural remodelling of the heart. This remodelling is a major cause of heart failure.

The researchers used a mouse model of high blood pressure to understand how nuclear pores contribute to this remodelling process. Mice that were engineered to express fewer nuclear pores showed less modulation of gene pathways involved in harmful cardiac remodelling. These mice also had better heart function and survival than their peers with more nuclear pores.

“We were surprised at the magnitude of the protective effect of having fewer nuclear pores in mice with high blood pressure,” said Prof Kühn. “However, having fewer communication pathways also limits beneficial signals such as those that promote regeneration.”

Source: University of Pittsburgh

Categories : Cardiovascular Disease COVIDTags :

Myocarditis Risk 7 Times Higher from COVID Infection than Vaccination

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According to a recent study published in Frontiers in Cardiovascular Medicine, the risk of developing myocarditis is seven times higher with a COVID infection than with the COVID vaccine, by scientists. Patients with myocarditis can experience chest pains, shortness of breath or an irregular heartbeat. In severe cases, the inflammation can lead to heart failure and death.

“Our findings show that the risk of myocarditis from being infected by COVID is far greater than from getting the vaccine,” said Dr Navya Voleti, a resident physician at Penn State College of Medicine. “Moving forward, it will be important to monitor the potential long-term effects in those who develop myocarditis.”

Typically resulting from viral infection, myocarditis is a known complication of SARS-CoV-2 infection, and heart complications have been associated with mRNA COVID vaccination – particularly myocarditis in teenage boys. However, the relative risk of myocarditis due to vaccines and infections had not been clearly established.

The researchers conducted the largest study to date on the risk of developing myocarditis as a result of SARS-CoV-2 infection vs experiencing inflammation after COVID vaccination. The researchers compared vaccinated and unvaccinated COVIP patients to uninfected controls. The myocarditis risk was 15 times higher in COVID patients, regardless of vaccination status, compared to individuals who did not contract the virus.

Next, the researchers separately compared the rates of myocarditis in those who received the vaccines to those in unvaccinated individuals. According to the findings, the rates of myocarditis in people who were vaccinated against COVID were only twofold higher than in unvaccinated people.

Based on all the findings, the researchers concluded that the risk of myocarditis due to COVID was seven times higher than the risk related to the vaccines.

Investigators conducted a systematic review and meta-analysis of 22 studies published worldwide from December 2019 through May 2022. The studies included nearly 58 million patients who reported cardiac complications and belonged to one of two groups: the 55.5 million who were vaccinated against COVID compared to those who were not vaccinated (vaccination group), and the 2.5 million who contracted the virus compared to those who did not contract the virus (COVID group).

In the vaccination group, the researchers separately compared the risk of myocarditis for various COVID vaccines. The median age of the study population was 49 years; 49% were men; and the median follow-up time after infection or COVID vaccination was 28 days.

The researchers found that among those diagnosed with myocarditis after receiving the vaccine or having COVID, the majority (61%) were men. Of patients diagnosed with myocarditis in both vaccination and COVID groups, 1.07% were hospitalised and 0.015% died.

“COVID infection and the related vaccines both pose a risk for myocarditis. However, the relative risk of heart inflammation induced by COVID infection is substantially greater than the risk posed by the vaccines,” said Dr. Paddy Ssentongo, a resident physician in the Department of Medicine at Penn State Health Milton S. Hershey Medical Center and the lead author of the study. “We hope our findings will help mitigate vaccine hesitancy and increase vaccine uptake.”

Source: Penn State

Categories : Cardiovascular Disease Substance UseTags :

Marijuana and other Substances Linked to Atrial Fibrillation

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A new longitudinal study of more than 23 million people in the US concludes that some commonly used and abused drugs pose previously unidentified risks for the development of atrial fibrillation (AF). The results appeared in the European Heart Journal.

The researchers analysed data from diagnostic codes from every hospital admission, emergency room visit and medical procedure in California for the years 2005 through 2015, identifying nearly one million people without preexisting AF, but who later developed AF during these years.

They found 132 834 patients used cannabis, 98 271 used methamphetamine, 48 700 used cocaine, and 10 032 used opiates. In the study, the researchers found that marijuana users had a 35% increased likelihood of later developing AF.

“Despite exhibiting a weaker association with incident AF than the other substances, cannabis use still exhibited an association of similar or greater magnitude to risk factors like dyslipidaemia, diabetes mellitus, and chronic kidney disease. Furthermore, those with cannabis use exhibited similar relative risk of incident AF as those with traditional tobacco use,” the study authors reported.

“To my knowledge, this is the first study to look at marijuana use as a predictor of future atrial fibrillation risk,” said principal investigator Gregory Marcus, MD, MAS, a UCSF professor of Medicine with the Division of Cardiology.

AF is an abnormally disordered pumping rhythm arising from electrical disturbances in the atria. In severe cases of faulty atrial pumping, clots may form in the atria, and then break off into the bloodstream and cause deadly strokes. AF-related strokes cause more than 150 000 US deaths each year.

Unlike cocaine or methamphetamine use, both stimulants previously known to sometimes lead to sudden cardiac death due to profound disruptions in the orderly electrical signalling and pumping within ventricles there is no demonstrated mechanism whereby marijuana use causes heart arrhythmias.

Source: University of California San Francisco

Categories : Cardiovascular Disease GenderTags :

Cardiovascular Disease Risk Factors the Same for Men and Women

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For men and women, the risk factors for cardiovascular disease are largely the same, an extensive global study involving over 155 000 participants shows.

The study, published in The Lancet, includes participants from 21 countries with differing GDP. Cardiovascular disease is more widespread in low- and middle-income countries.

The 21-country study used data were taken from the Prospective Urban Rural Epidemiological (PURE) Study and comprised 155 724 participants aged 35–70 years with no history of cardiovascular disease when they joined the study. All cases of fatal cardiovascular disease, heart attack, stroke, and heart failure during the follow-up period, which averaged ten years, were registered.

The risk factors studied were metabolic (such as high blood pressure, obesity, and diabetes), behavioral (tobacco smoking and diet), and psychosocial (economic status and depression).

No clear gender or income divide

Metabolic risk factors were found to be similar in both sexes, except for high values of low-density lipoprotein (LDL, often known as bad cholesterol), where the association with cardiovascular disease was stronger in men. In the researchers’ opinion, however, this finding needs confirmation in more studies.

Depressive symptoms were another risk factor for cardiovascular disease that proved to be more significant among the men than the women. On the other hand, the link between a poor diet and cardiovascular disease was closer in women; and smoking, though markedly more frequent among men, was just as injurious a risk factor for women.

Overall, the researchers found broadly similar risk factors for cardiovascular disease for the male and female participants, irrespective of their countries’ income level. This highlights the importance of disease prevention strategies, too, being the same for both sexes.

Similarities greater than differences

The women’s lower overall risk of cardiovascular disease, especially heart attack (myocardial infarction), may be explained by the younger women’s higher tolerance to risk factors. Their estrogen makes vessel walls more compliant and affects the liver’s capacity to get rid of LDL.

Among the 90 934 women in the study, 5.0 cases of stroke, heart attack, and/or cardiovascular disease were registered per 1000 persons per year. The corresponding number in the group of men (64 790 individuals) was 8.2 cases.

Annika Rosengren, Professor of Medicine at Sahlgrenska Academy, University of Gothenburg, is the second author of the study, in charge of the Swedish part of the PURE population study of 4 000 individuals in Gothenburg and Skaraborg.

“When it comes to cardiovascular disease in men and women, the similarities in terms of risk factors are considerably greater than the differences. But men are more vulnerable to high levels of LDL, the bad cholesterol, and we know from other studies that they develop pathological changes in the coronary arteries at a lower age than women, and tend to start developing myocardial infarction quite a lot earlier. With respect to early stroke, though, the sex differences are less pronounced, as we’ve also seen in other studies,” Prof Rosengren said.

Source: University of Gothenburg

Categories : Cardiovascular Disease GenderTags :

Sex Differences in Post-stroke Biomarkers

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Credit: American Heart Association

Although males and females are equally affected by stroke Since oestrogen and progesterone have known neuroprotective effects, it is important to compare the size, severity and biochemical composition of the brain tissue following stroke in female and male animal models. In a paper published in IBRO Neuroscience Reports, researchers have discovered that certain biomarkers were different in the brains of male and female mice.

Stroke neurosurgeon and research coordinator Prof Nicole Sylvain and her colleagues are looking at treatments for post-stroke recovery that help supplement these energy losses. Using the Canadian Light Source (CLS) at the University of Saskatchewan (USask), the team was able to identify energy biomarkers in the brain, which could eventually inform clinicians about the effects of potential stroke treatments on brain recovery after a stroke.

The group’s recent study examined post-stroke differences between male and female mice, and found that female mice have higher amounts of glycogen in their brains. Glycogen is a sugar-like substance that circulates in our blood and nourishes our cells. When the supply of glycogen is disrupted by stroke, the brain is severely impacted.

Most pre-clinical stroke research has been performed using male lab animals, with results usually generalised to both sexes. In clinical stoke cases, females have a higher incidence of ischaemic stroke and poorer outcomes, compared to males.

“We found that, for the most part, male data can be generalised for females, however, some of the metabolic markers we measured were actually different,” Sylvain said. “It’s really important to do the research on both sexes.”

It would be impossible for the team to detect the biomarkers without to the Mid-IR beamline.

“The only way to detect them in such an accurate way across the brain is with infrared imaging, so the CLS has been absolutely vital to our research.”

Source: University of Saskatchewan

Categories : Cardiovascular Disease Medical Research & TechnologyTags :

Discovery Could Lead to Blood Pressure Drugs with Fewer Side Effects

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Researchers at the University of Virginia have identified a key contributor to hypertension that could lead to new treatments with fewer side effects. Their findings were published in the journal Circulation.

The discovery, from scientist Swapnil Sonkusare, PhD, and colleagues, sheds new light on blood pressure regulation and how problems with this critical biological process drive hypertension.

Blood pressure is partly controlled by calcium levels in smooth muscle cells that line blood vessel walls. Smooth muscle cells take in calcium and use it to regulate the contraction of blood vessels as needed. Hypertension is commonly treated with calcium blockers that reduce the movement of calcium, but since multiple organs also use this calcium mechanism, these drugs have many side effects. So a treatment option that targets the harmful effects of calcium but not its beneficial effects could be very helpful for patients with hypertension.

Dr Sonkusare and his team discovered two critical signalling centres in smooth muscle cells that bring in calcium and regulate blood pressure. These ‘nanodomains’, the researchers found, act like symphony conductors for blood vessels, directing them to contract or relax as needed. These signalling centres, the researchers determined, are a key regulator of healthy blood pressure.

Further, the UVA scientists found that disruptions in this process contribute to high blood pressure. In both mouse models of the disease and hypertensive patients, the fine balance between constrictor and dilator signalling centres is lost. This caused the blood vessels to become too constricted, driving up blood pressure.

“Our work identifies a new mechanism that helps maintain healthy blood pressure and shows how abnormalities in this mechanism can lead to hypertension,” said Dr Sonkusare. “The discovery of a new mechanism for elevation of blood pressure could provide therapeutic targets for treating hypertension.”

The research identifies a “new paradigm in hypertension,” according to an accompanying editorial. The editorial says UVA’s “innovative” discoveries fill “major gaps” in our understanding of the fundamental molecular causes of high blood pressure.

The new findings help us better understand how our bodies maintain proper blood pressure and provide enticing targets for scientists seeking to develop treatments targeting underlying causes of hypertension. Developing treatments that do not affect the beneficial effects of calcium will require additional research and a deeper understanding of the calcium-use process, but Dr Sonkusare’s team is already working toward that goal.

“We’ve shown that smooth muscle cells use ‘spatial separation’ of signalling centres to achieve constriction or dilation of arteries. We are now investigating the individual components of these signalling centres,” Dr Sonkusare said. “Understanding these components will help us target them to lower or raise the blood pressure in disease conditions that show high or low blood pressure, respectively.”

Source: University of Virginia

Categories : Cardiovascular Disease COVIDTags :

Paxlovid may Interact with Common Heart Drugs

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Nirmatrelvir-ritonavir (Paxlovid) is often given to heart disease patients with symptomatic COVID to prevent progression to severe disease – but it can interact with some previously prescribed medications. A review paper published in the Journal of the American College of Cardiology examines the potential drug-drug interactions (DDIs) between Paxlovid and commonly used cardiovascular medications, as well as potential options to mitigate severe adverse effects.

“Awareness of the presence of drug-drug interactions of Paxlovid with common cardiovascular drugs is key. System-level interventions by integrating drug-drug interactions into electronic medical records could help avoid related adverse events,” said Sarju Ganatra, MD, senior author of the review.

He continued: “The prescription of Paxlovid could be incorporated into an order set, which allows physicians, whether it be primary care physicians or cardiology providers, to consciously rule out any contraindications to the co-administration of Paxlovid. Consultation with other members of the health care team, particularly pharmacists, can prove to be extremely valuable. However, a health care provider’s fundamental understanding of the drug-drug interactions with cardiovascular medications is key.”

In December 2021, Paxlovid received emergency use authorisation from the US Food and Drug Administration as an oral antiviral agent for the treatment of symptomatic, non-hospitalised adults with mild to moderate COVID infection who are at high risk for progression to severe disease. Patients with heart disease and other risk factors, including diabetes, high blood pressure, chronic kidney disease and smoking make up a large portion of the high-risk population for whom Paxlovid is beneficial.

According to the authors, Paxlovid has been shown to be very effective in patients with existing heart disease, but it has significant DDIs with commonly used cardiovascular medications, highlighting the importance for all clinicians to be familiar with these DDIs. As there is limited clinical information regarding DDI-related adverse events, the authors used existing knowledge and data regarding how therapies like Paxlovid typically react with other medications to provide guidance regarding potential interactions and the associated likely consequences based on the degree of interaction.

The review provides an in-depth overview of a variety of cardiovascular medications used to treat many forms of heart disease. Five of the most important cardiovascular drug interactions with Paxlovid to be aware of include:

  • Anti-arrhythmic agents
    • Many anti-arrhythmic agents are metabolised in a way that increases plasma levels when co-administered with Paxlovid. While it may be possible to start Paxlovid after 2–2.5-day temporary discontinuation of the anti-arrhythmic agents, this may not be feasible from a practical standpoint. Clinicians are advised to consider alternative COVID therapies and avoid co-administration of these agents with Paxlovid. Sotalol, another anti-arrhythmic agent, is renally cleared and does not interact with Paxlovid.
  • Antiplatelet agents and anticoagulants
    • Antiplatelet agents are used for the treatment of coronary artery disease, particularly if a patient has received a stent. Aspirin and prasugrel are safe to co-administer with Paxlovid. There is an increased risk of blood clots when Paxlovid is given alongside clopidogrel and an increased risk of bleeding when given with ticagrelor. When possible, these agents should be switched to prasugrel. If patients have contraindication to taking prasugrel, then co-administration of Paxlovid should be avoided and alternative COVID therapies should be considered.
    • Anticoagulants such as warfarin may be co-administered with Paxlovid but require close monitoring of clotting factors in bloodwork. The plasma levels of all direct oral anticoagulants increase when co-administered with Paxlovid, therefore dose adjustment or temporary discontinuation and use of alternative anticoagulants may be required.
  • Certain statins
    • Co-administration of simvastatin or lovastatin with Paxlovid can lead to increased plasma levels and subsequent myopathy and rhabdomyolysis, a condition in which the breakdown of muscle tissue releases a damaging protein into the bloodstream. These agents should be stopped prior to initiation of Paxlovid. A dose reduction of atorvastatin and rosuvastatin is reasonable when co-administered with Paxlovid. The other statins are considered safe when given along with Paxlovid.
  • Ranolazine
    • Plasma concentration of ranolazine, used to treat angina and other heart-related chest pain, is exponentially increased in the presence of CPY450 inhibitors like Paxlovid, thereby increasing the risk of clinically significant QT prolongation and torsade de pointes (a type of arrhythmia). Co-administration of Paxlovid is therefore contraindicated. Temporary discontinuation of ranolazine is advised if prescribing Paxlovid.
  • Immunosuppressive agents
    • The plasma levels of immunosuppressive agents prescribed for patients who have undergone heart transplantation exponentially rise to toxic levels when co-administered with Paxlovid. Temporary reduction of dosing of immunosuppressive agents would require frequent monitoring and be logistically difficult. Therefore, alternative COVID therapies should be considered in these patients.

The authors conclude awareness and availability of other COVID therapies enable clinicians to offer alternative treatment options to patients who are unable to take Paxlovid due to DDIs.

Categories : Cardiovascular DiseaseTags :

Could Metformin be Used to Treat Atrial Fibrillation?

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Cleveland Clinic researchers have identified metformin as a possible treatment for atrial fibrillation (AF). In the study, published in Cell Reports Medicine, researchers used advanced computation and genetic sequencing to determine that metformin’s targets overlap significantly with genes that are dysregulated in AF.

“Finding drugs or procedures to treat atrial fibrillation is difficult because of potential serious side effects,” said Mina Chung, MD, senior study author. “There is a significant need for new treatments for atrial fibrillation as there have been no new drugs approved in more than a decade.”

“It’s not that we’ve found a new drug target where it takes 20 years to test this in individuals,” said Jessica Castrillon Lal, first author and graduate student.

“We can cut off 10+ years in the drug development pipeline. We already have the information there. We just have to test it in a very computationally efficient way, such as artificial intelligence technology,” said Feixiong Cheng, PhD, co-senior study author.

The analysis found metformin targeted 30 genes associated with AF, with direct effects on gene expression for eight. Eight other candidate drugs surfaced in the analysis, but further testing and patient data review identified metformin as the most promising candidate.

Castrillon Lal conducts research in Dr Cheng’s lab, which uses network medicine approaches to find candidate drugs for repurposing, creating vast networks of molecular interactions. For this study, researchers narrowed down a list of 2800 FDA-approved treatments by analysing three data sources: a map of interactions between proteins called an “interactome”; a network of genes associated with atrial fibrillation; and each medicine’s molecular or genetic targets.

Atrial fibrillation is the most common type of heart arrhythmia in the world and can lead to complications, including stroke and heart failure. Treatments have been primarily directed toward trying to prevent the arrhythmia using drugs targeting the electrical system, including ion channels in the heart, or using catheter ablation to isolate the pulmonary veins where initiating beats of atrial fibrillation occur.

However, side effects, limited success and potential complications can limit these approaches.

Source: Cleveland Clinic

Categories : Cardiovascular Disease PaediatricsTags :

Arrhythmias From Playing Video Games in Susceptible Children

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Video games can precipitate life-threatening cardiac arrhythmias in susceptible children whose predisposition may have been previously unrecognised, according to findings published in Heart Rhythm. The investigators documented an uncommon, but distinct pattern among children who lose consciousness while playing video games – particularly among multiplayer war gaming which can have stressful online interactions.

“Video games may represent a serious risk to some children with arrhythmic conditions; they might be lethal in patients with predisposing, but often previously unrecognized arrhythmic conditions,” explained lead investigator Claire M. Lawley, MBBS, PhD. “Children who suddenly lose consciousness while electronic gaming should be assessed by a heart specialist as this could be the first sign of a serious heart problem.”

The investigators performed a systematic review of literature and initiated a multisite international outreach effort to identify cases of children with sudden loss of consciousness while playing video games. Across the 22 cases found, multiplayer war gaming was the most frequent trigger, and some children died following a cardiac arrest. Subsequent diagnoses of several heart rhythm conditions put the children at continuing risk. Catecholaminergic polymorphic ventricular tachycardia (CPVT) and congenital long QT syndrome (LQTS) types 1 and 2 were the most common underlying causes.

There was a high incidence of potentially relevant genetic variants (63%) among the patients, which has significant implications for their families. In some cases, the investigation led to the diagnosis of familial heart problems. “Families and healthcare teams should think about safety precautions around electronic gaming in children who have a condition where dangerous fast heart rhythms are a risk,” noted Dr Lawley.

Adrenergic stimulation related to the emotionally charged electronic gaming environment was attributed as the pathophysiological basis for this phenomenon. At the time of the cardiac incidents, many of the patients were in excited states, having just won or lost games, or were engaging in conflict with companions.

“We already know that some children have heart conditions that can put them at risk when playing competitive sports, but we were shocked to discover that some patients were having life-threatening blackouts during video gaming,” added co-investigator Christian Turner, MBBS. “Video gaming was something I previously thought would be an alternative ‘safe activity.’ This is a really important discovery. We need to ensure everyone knows how important it is to get checked out when someone has had a blacking out episode in these circumstances.”

The study notes that while this phenomenon is not a common occurrence, it is becoming more prevalent. “Having looked after children with heart rhythm problems for more than 25 years, I was staggered to see how widespread this emerging presentation is, and to find that a number of children had even died from it. All of the collaborators are keen to publicize this phenomenon so our colleagues across the globe can recognize it and protect these children and their families,” noted co-investigator of the study, Jonathan Skinner, MBChB, MD, also from Sydney.

In an accompanying editorial Daniel Sohinki, MD, MSc, and coauthors pointed out that, “exertion should be understood to encompass activities outside of traditional competitive athletics. Appropriate counselling regarding the risks of intense video gameplay should be targeted in children with a pro-arrhythmic cardiac diagnosis, and in any child with a history of exertional syncope of undetermined aetiology. Further, any future screening programs aimed at identifying athletes at risk for malignant arrhythmias should encompass athletes being considered for participation in eSports.”

Source: EurekAlert!

Categories : Cardiovascular Disease Obstetrics & GynaecologyTags :

Study Demonstrates Safer Preeclampsia Treatment with Nifedipine

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Image by Hush Naidoo from Unsplash
Image by Hush Naidoo from Unsplash

Women with severe preeclampsia may be treated with extended-release nifedipine, a blood pressure-lowering medicine, daily during the labour and delivery process, according to new research published today in Hypertension. Women receiving the drug had a lower risk of dangerously high blood pressure that would require treatment with fast-acting medicines including intravenous (IV) medications.

The study examined whether treatment with nifedipine, an extended-release blood pressure-lowering medication, leading up to labour and delivery may prevent severe blood pressure levels from developing, and, as a result, avoid the need to administer fast-acting IV medications.

According to the American Heart Association, preeclampsia is typically diagnosed after 20 weeks of pregnancy and indicates high blood pressure measures with symptoms such as headaches, vision changes and swelling of the hands, feet, face or eyes. It affects up to 8% of pregnancies. A diagnosis of preeclampsia with severe features typically includes systolic BP of ≥ 160mmHg and/or diastolic BP ≥ 110mmHg, and proteinuria. It increases the risk of stroke, liver or kidney damage and pre-term delivery. Delivery of the baby is the only way to start to cure preeclampsia, and symptoms usually go away within days of delivery. However, some women require BP medication for six weeks after delivery or longer.

“We know that bringing down very high blood pressure to a safer range will help prevent maternal and foetal complications. However, besides rapid-acting, IV medicines for severe hypertension during pregnancy, optimal management for hypertension during the labour and delivery process, has not been studied,” said lead study author Erin M. Cleary, MD.

Sever hypertension also raises the risk for complications such as placental abruption, leading to serious complications for mother and/or the baby.

“Some of these complications may include emergency delivery, blood loss for the mother and may be life threatening for both the mother and baby,” Dr Cleary said. “About 10% of patients treated with a rapid-IV treatment for very high blood pressure may quickly have very low blood pressures. When blood pressure gets too low, too fast, that can lead to other serious complications.”

The study was conducted from June 2020 to April 2022 at The Ohio State University Wexner Medical Center and included 110 women who were at least 22 weeks pregnant, diagnosed with severe preeclampsia and who underwent induction of labour. Half were randomised to take a 30mg oral pill nifedipine extended-release once a day until delivery, the other half took a placebo pill daily until delivery. Participants were followed through hospital discharge, and chart review was performed through six weeks postpartum to monitor for any postpartum readmissions along with reasons for readmission.

The researchers also examined the impact of nifedipine treatment on delivery, if and how long the baby may have needed care in the neonatal intensive care unit (NICU) and other adverse outcomes for the mother and/or baby.

The study found:

  • 34% of women in the nifedipine group needed acute hypertension therapy compared to 55.1% of those in the placebo group.
  • There were fewer Caesarean deliveries among the women treated with nifedipine: 20.8% of women in the nifedipine treatment group had a Caesarean section, compared to 34.7% of women in the placebo group.
  • The rate of NICU admission for the newborns was lower if the mother was treated with nifedipine (29.1%) compared to the placebo group (47.1%).
  • Poor outcomes for the infant – such as lower Apgar score, low blood sugar levels, high bilirubin or needing extra oxygen – did not differ significantly between the two treatment groups.

It’s important to note, however, that the number of participants in this study was too small to determine whether the differences in the NICU and Caesarean rates may hold true or if they may be due to chance or other factors. The researchers plan to conduct larger studies with more participants to better understand if these differences are valid.

Source: American Heart Association