Comparison of global estimates of prevalence and risk factors for peripheral artery disease in 2000 and 2010: a systematic review and analysis.


Background

Lower extremity peripheral artery disease is the third leading cause of atherosclerotic cardiovascular morbidity, following coronary artery disease and stroke. This study provides the first comparison of the prevalence of peripheral artery disease between high-income countries (HIC) and low-income or middle-income countries (LMIC), establishes the primary risk factors for peripheral artery disease in these settings, and estimates the number of people living with peripheral artery disease regionally and globally.

Methods

We did a systematic review of the literature on the prevalence of peripheral artery disease in which we searched for community-based studies since 1997 that defined peripheral artery disease as an ankle brachial index (ABI) lower than or equal to 0·90. We used epidemiological modelling to define age-specific and sex-specific prevalence rates in HIC and in LMIC and combined them with UN population numbers for 2000 and 2010 to estimate the global prevalence of peripheral artery disease. Within a subset of studies, we did meta-analyses of odds ratios (ORs) associated with 15 putative risk factors for peripheral artery disease to estimate their effect size in HIC and LMIC. We then used the risk factors to predict peripheral artery disease numbers in eight WHO regions (three HIC and five LMIC).

Findings

34 studies satisfied the inclusion criteria, 22 from HIC and 12 from LMIC, including 112 027 participants, of which 9347 had peripheral artery disease. Sex-specific prevalence rates increased with age and were broadly similar in HIC and LMIC and in men and women. The prevalence in HIC at age 45—49 years was 5·28% (95% CI 3·38—8·17%) in women and 5·41% (3·41—8·49%) in men, and at age 85—89 years, it was 18·38% (11·16—28·76%) in women and 18·83% (12·03—28·25%) in men. Prevalence in men was lower in LMIC than in HIC (2·89% [2·04—4·07%] at 45—49 years and 14·94% [9·58—22·56%] at 85—89 years). In LMIC, rates were higher in women than in men, especially at younger ages (6·31% [4·86—8·15%] of women aged 45—49 years). Smoking was an important risk factor in both HIC and LMIC, with meta-OR for current smoking of 2·72 (95% CI 2·39—3·09) in HIC and 1·42 (1·25—1·62) in LMIC, followed by diabetes (1·88 [1·66—2·14] vs 1·47 [1·29—1·68]), hypertension (1·55 [1·42—1·71] vs 1·36 [1·24—1·50]), and hypercholesterolaemia (1·19 [1·07—1·33] vs 1·14 [1·03—1·25]). Globally, 202 million people were living with peripheral artery disease in 2010, 69·7% of them in LMIC, including 54·8 million in southeast Asia and 45·9 million in the western Pacific Region. During the preceding decade the number of individuals with peripheral artery disease increased by 28·7% in LMIC and 13·1% in HIC.

Interpretation

In the 21st century, peripheral artery disease has become a global problem. Governments, non-governmental organisations, and the private sector in LMIC need to address the social and economic consequences, and assess the best strategies for optimum treatment and prevention of this disease.

Source: Lancet.

 


What causes coronary heart disease?

Coronary heart disease (CHD) is arguably the the UK’s biggest killer. CHD develops when the blood supply to the muscles and tissues of the heart becomes obstructed by the build-up of fatty materials inside the walls of the coronary arteries.

heart

What is coronary heart disease?

Your heart is a pump the size of a fist that sends oxygen-rich blood around your body. The blood travels to the organs of your body through blood vessels known as arteries, and returns to the heart through veins.

Your heart needs its own blood supply to keep working. Heart disease occurs when the arteries that carry this blood, known as coronary arteries, start to become blocked by a build-up of fatty deposits.

How common is CHD?

  • CHD causes round 74,000 deaths each year. That’s an average of 200 people every day
  • In the UK, there are an estimated 2.3 million people living with the condition
  • About one in six men and one in nine women die from the disease
  • Death rates are highest in Scotland and northern England
  • In the past couple of decades, deaths from CHD have nearly halved due to better treatments

Source: British Heart Foundation

The inner lining of the coronary arteries gradually becomes furred with a thick, porridge-like sludge of substances, known as plaques, and formed from cholesterol. This clogging-up process is known as atherosclerosis.

The plaques narrow the arteries and reduce the space through which blood can flow. They can also block nutrients being delivered to the artery walls, which means the arteries lose their elasticity. In turn, this can lead to high blood pressure, which also increases the risk of heart disease. This same process goes on in the arteries throughout the body, and can lead to high blood pressure which puts further strain on the heart.

If your arteries are partially blocked you can experience angina – severe chest pains that can spread across your upper body – as your heart struggles to keep beating on a restricted supply of oxygen. You are also at greater risk of a heart attack.

Some people have a higher risk of developing atherosclerosis due to genetic factors – one clue to this is a family history of heart disease in middle-age. Lifestyle factors that increase the risk include an unhealthy diet, lack of exercise, diabetes, high blood pressure and, most importantly, smoking.

However, in the past couple of decades deaths from coronary heart disease have nearly halved, thanks to better treatments.

What happens during a heart attack?

A heart attack happens when one of the coronary arteries becomes completely blocked. This usually happens when a plaque, which is already narrowing an artery, cracks or splits open. This triggers the formation of a blood clot around the plaque, and it is this blood clot that then completely blocks the artery.

With their supply of oxygen completely blocked, the heart muscle and tissue supplied by that artery start to die. Emergency medical intervention is needed to unblock the artery and restore blood flow. This may consist of treatment with drugs to dissolve the clot or thrombus, or a small operation done through the skin and blood vessels to open up the blocked artery.

The outcome of a heart attack hinges on the amount of the muscle that dies before it is corrected. The smaller the area affected, the greater the chance of survival and recovery.

While a heart attack will always cause some permanent damage, some areas may be able to recover if they are not deprived of blood for too long. The sooner a heart attack is diagnosed and treated, the greater the chance of recovery.

Other heart diseases

Other diseases that commonly affect the heart include:

  • Chronic heart failure – CHD is one of the main causes of heart failure. It affects around one million people in the UK, and many more have it but haven’t been formally diagnosed. Here, the heart doesn’t works effectively as a pump, and fluid gathers in the lower limbs and lungs. This causes a variety of symptoms and significantly reduces quality of life.
  • Infection – bacterial infections such as endocarditis are much rarer these days thanks to antibiotics, but can damage the valves of the heart as well as other tissues. Viral infections can damage the heart muscle leading to heart failure, or cause abnormal heart rhythms.
  • Congenital heart disease – a number of defects can develop in the heart as a baby grows in the womb. One example is a hole in the heart, also known as a septal defect. Congenital heart disease may cause abnormal blood flow and put excessive strain on the infant’s heart after it has been born.
  • Cardiomyopathy – a disease of the heart muscle that can occur for different reasons, including coronary heart disease, high blood pressure, viral infection, high alcohol intake and thyroid disease.

Source: BBC

 

What causes coronary heart disease?


_67019810_heart122375065

Coronary heart disease (CHD) is arguably the the UK’s biggest killer. CHD develops when the blood supply to the muscles and tissues of the heart becomes obstructed by the build-up of fatty materials inside the walls of the coronary arteries.

What is coronary heart disease?

Your heart is a pump the size of a fist that sends oxygen-rich blood around your body. The blood travels to the organs of your body through blood vessels known as arteries, and returns to the heart through veins.

Your heart needs its own blood supply to keep working. Heart disease occurs when the arteries that carry this blood, known as coronary arteries, start to become blocked by a build-up of fatty deposits.

How common is CHD?

  • CHD causes round 74,000 deaths each year. That’s an average of 200 people every day
  • In the UK, there are an estimated 2.3 million people living with the condition
  • About one in six men and one in nine women die from the disease
  • Death rates are highest in Scotland and northern England
  • In the past couple of decades, deaths from CHD have nearly halved due to better treatments

Source: British Heart Foundation

The inner lining of the coronary arteries gradually becomes furred with a thick, porridge-like sludge of substances, known as plaques, and formed from cholesterol. This clogging-up process is known as atherosclerosis.

The plaques narrow the arteries and reduce the space through which blood can flow. They can also block nutrients being delivered to the artery walls, which means the arteries lose their elasticity. In turn, this can lead to high blood pressure, which also increases the risk of heart disease. This same process goes on in the arteries throughout the body, and can lead to high blood pressure which puts further strain on the heart.

If your arteries are partially blocked you can experience angina – severe chest pains that can spread across your upper body – as your heart struggles to keep beating on a restricted supply of oxygen. You are also at greater risk of a heart attack.

Some people have a higher risk of developing atherosclerosis due to genetic factors – one clue to this is a family history of heart disease in middle-age. Lifestyle factors that increase the risk include an unhealthy diet, lack of exercise, diabetes, high blood pressure and, most importantly, smoking.

However, in the past couple of decades deaths from coronary heart disease have nearly halved, thanks to better treatments.

What happens during a heart attack?

A heart attack happens when one of the coronary arteries becomes completely blocked. This usually happens when a plaque, which is already narrowing an artery, cracks or splits open. This triggers the formation of a blood clot around the plaque, and it is this blood clot that then completely blocks the artery.

With their supply of oxygen completely blocked, the heart muscle and tissue supplied by that artery start to die. Emergency medical intervention is needed to unblock the artery and restore blood flow. This may consist of treatment with drugs to dissolve the clot or thrombus, or a small operation done through the skin and blood vessels to open up the blocked artery.

The outcome of a heart attack hinges on the amount of the muscle that dies before it is corrected. The smaller the area affected, the greater the chance of survival and recovery.

While a heart attack will always cause some permanent damage, some areas may be able to recover if they are not deprived of blood for too long. The sooner a heart attack is diagnosed and treated, the greater the chance of recovery.

Other heart diseases

Other diseases that commonly affect the heart include:

  • Chronic heart failure – CHD is one of the main causes of heart failure. It affects around one million people in the UK, and many more have it but haven’t been formally diagnosed. Here, the heart doesn’t works effectively as a pump, and fluid gathers in the lower limbs and lungs. This causes a variety of symptoms and significantly reduces quality of life.
  • Infection – bacterial infections such as endocarditis are much rarer these days thanks to antibiotics, but can damage the valves of the heart as well as other tissues. Viral infections can damage the heart muscle leading to heart failure, or cause abnormal heart rhythms.
  • Congenital heart disease – a number of defects can develop in the heart as a baby grows in the womb. One example is a hole in the heart, also known as a septal defect. Congenital heart disease may cause abnormal blood flow and put excessive strain on the infant’s heart after it has been born.
  • Cardiomyopathy – a disease of the heart muscle that can occur for different reasons, including coronary heart disease, high blood pressure, viral infection, high alcohol intake and thyroid disease.

Source: BBC

 

 

Magnetic resonance angiography of intracranial and extracranial arteries in patients with spontaneous migraine without aura: a cross-sectional study.


Background

Extracranial arterial dilatation has been hypothesised to be the cause of pain in patients who have migraine without aura. To test that hypothesis, we aimed to measure extracranial and intracranial arteries during attacks of migraine without aura.

Methods

In this cross-sectional study, we recruited patients aged 18—60 years from the Danish Headache Centre and via announcements on a Danish website. We did magnetic resonance angiography during spontaneous unilateral migraine attacks. Primary endpoints were difference in circumference of extracranial and intracranial arterial segments comparing attack and attack-free days and the pain and the non-pain side. The extracranial arterial segments measured were the external carotid (ECA), the superficial temporal (STA), the middle meningeal (MMA), and the cervical part of the internal carotid (ICAcervical) arteries. The intracranial arterial segments were the cavernous (ICAcavernous) and cerebral (ICAcerebral) parts of the internal carotid, the middle cerebral (MCA), and the basilar (BA) arteries. This study is registered atClinicaltrials.gov, number NCT01471314.

Findings

Between Oct 12, 2010, and Feb 8, 2012, we recruited 78 patients, of whom 19 women had a scan during migraine and were included in the final analysis. On migraine compared with non-migraine days, we detected no statistically significant dilatation of the extracranial arteries on the pain side (ECA, mean difference 1·2% [95% CI −5·7 to 8·2] p=0·985, STA 3·6% [—3·7 to 11·0] p=0·532, MMA 1·7% [—1·7 to 5·2] p=0·341, and ICAcervical 2·3% [—0·3 to 4·9] p=0·093); the intracranial arteries were more dilated during attacks (MCA, 13·0% [6·4 to 19·6] p=0·001, ICAcerebral 11·5% [5·6 to 17·3] p=0·0004, and ICAcavernous 11·4% [5·3 to 17·5] p=0·001), except for the BA (1·6% [—2·7 to 5·9] p=0·621). Compared with the non-pain side, during attacks we detected dilatation on the pain side of the intracranial arteries (MCA, mean difference 10·5% [0·7—20·3] p=0·044, ICAcerebral (14·4% [4·6—24·1] p=0·013), and ICAcavernous (9·1% [3·9—14·4] p=0·003) but not of the extracranial arteries (ECA, 2·1% [—3·8 to 9·2] p=0·238, STA, 3·6% [—3·7 to 10·8] p=0·525, MMA, 2·7% [—1·3 to 5·6] p=0·531, and ICAcervical, 5·0% [—0·5 to 10·4] p=0·119).

Interpretation

Migraine pain was not accompanied by extracranial arterial dilatation, and by only slight intracranial dilatation. Future migraine research should focus on the peripheral and central pain pathways rather than simple arterial dilatation.

Source: Lancet

 

Structural and biochemical characteristics of arterial stiffness in patients with atherosclerosis and in healthy subjects.


Arterial stiffness is an independent predictor of vascular morbidity and mortality in patients with atherosclerosis. Angiographic score (ASc) reflects severity of atherosclerosis in patients with peripheral arterial disease (PAD). Osteopontin (OPN) and oxidized low-density lipoprotein (oxLDL) are involved in the pathogenesis of atherosclerosis. The aim of the present study was to evaluate the association between arterial stiffness, ASc, serum OPN and oxLDL in patients with symptomatic PAD, and in clinically healthy subjects. We studied 79 men with symptomatic PAD (mean age 64±7 years) and 84 healthy men (mean age 63±8 years). Calculation of the ASc was based on severity and location of atherosclerotic lesions in the arteries of the lower extremities. Aortic pulse wave velocity (aPWV) was evaluated by applanation tonometry using the Sphygmocor device. Serum OPN and oxLDL levels were determined by enzyme-linked immunosorbent assay. The aPWV (10±2.4 VS. 8.4±1.7 (m s−1); P<0.001), OPN (75 (62.3–85.8) VS. 54.8 (47.7–67.9) (ng ml−1); P<0.001) and oxLDL (67 (52.5–93.5) VS. 47.5 (37–65.5); P<0.001) were different for the patients and for the controls. In multiple regression models, aPWV was independently determined by ASc, log-OPN, log-oxLDL and estimated glomerular filtration rate in the patients (R2=0.44; P<0.001) and by log-OPN, log-oxLDL, age and heart rate in the controls (R2=0.38; P<0.001). The independent relationship of a PWV with serum levels of OPN and oxLDL in the patients with PAD and in the controls indicates that OPN and oxLDL might influence arterial stiffening in patients with atherosclerosis and in clinically healthy subjects.

Source: Hypertension Research/nature.