We all know people who seem to have been born with good genes—they may smoke, never exercise, or consume large amounts of bacon, yet they remain seemingly healthy. Now, researchers have found that individuals who carry a rare genetic mutation that controls the blood levels of certain fats, or lipids, are protected from heart disease. The result, reported here yesterday at the annual meeting of the American Society of Human Genetics, suggests that a drug mimicking this effect could prevent heart disease, a major killer.
High sodium intake as a source of high blood pressure has been an unchallenged dogmatic mantra for decades. But a few renegade MDs, several naturopaths, and chiropractors have challenged the unproven hypothesis of salt being the basis of high blood pressure (HBP). Turns out that the link between high sodium intake and elevated blood pressure is a false one.
Pure, unrefined salt is actually a necessary and helpful dietary component. Perhaps the most well known salt promoter is Dr. David Brownstein, MD, author of Salt Your Way to Health. Refined commercial table salt, used excessively in processed foods, is processed with toxic chemicals and stripped of its inherent nutritional value. It’s mostly poison with very little nutrition, though even using table salt often won’t lead to high blood pressure.
Actually, those with high blood pressure (and everyone, really) should just consume more foods rich in potassium. Meta-analysis’ show how low potassium intake has the same impact on blood pressure as high salt consumption – the real problem is an imbalance between sodium and potassium.
HFCS is more commonly used in processed foods, fruit juices, sweets, and sodas than cane or beet sugar. It’s cheaper than sucrose (table sugar), and satisfies the “sweet tooth” SAD (standard American diet) consumers’ desire.
According to the USDA, HFCS consumption has increased significantly from 1970 to 2005, and it is now the number one source of empty calories in America. In fact, Americans eat approximately 35 lbs on average of high-fructose corn syrup each year.
How HFCS Contributes to Hypertension or High Blood Pressure
Fructose in fruit is tied to several other nutritional compounds that balance out fructose’s negative aspects. But fructose isolated from corn and made into a syrup is too much for the body to metabolize. Even table sugar metabolizes better.
Robert H. Lustig, MD, a Professor of Pediatrics in the Division of Endocrinology, explains how the rise in HFCS use over the past three to four decades is behind the obesity and diabetes epidemic, both of which contribute to high blood pressure.
HFCS or “corn sugar” or “corn syrup” initiates a toxic overload from insufficient metabolism. The liver doesn’t convert isolated, concentrated fructose into energy well and stores it as fat instead. Add this to the dangers of GMO corn with traces of extremely toxic glyphosate herbicides and mercury as a byproduct from the conversion process. This toxic overload leads to obesity, fatty liver, other liver complications, and kidney disease.
Dr. Richard Johnson of the University of Colorado has been a researcher of investigations into HFCS and high blood pressure. His research revealed definite links of high HFCS consumption to high blood pressure.
What’s more, one of the toxic waste products remaining in the body from regular HFCS consumption is uric acid. A test of 17 subjects with high uric acid counts showed all 17 with high blood pressure. Uric acid inhibits nitric oxide (NO) in the blood vessels.
Nitric oxide is a volatile gas that helps maintain blood vessel elasticity. When that elasticity decreases, blood pressure increases. Here are 4 ways to increase nitric oxide naturally.
A safe range of uric acid is from 3 to 5.5 milligrams per deciliter (0.1 liter), with 4 mg/dl ideal for men and 3.5 mg/dl for women. Higher numbers threaten blood pressure increases. You can ask your health professional about a uric acid test or shop the internet by inserting “uric acid blood testing” in your search engine.
A 48-year-old man was referred to our institution because of shortness of breath and symptoms related to right ventricular dysfunction.
His medical history included tuberculosis as a child. Chest radiography showed a calcific ring located at the heart base. Transthoracic echocardiography showed signs of cardiac tamponade. High resolution CT scan showed the calcific ring at the cardiac base reproducing “el corazón espinado” (the sacred heart wrapped in thorns), with incomplete compression at the level of the inferior vena cava. The patient underwent successful pericardectomy (removal of the pericardium). Despite repeated attempts, the diaphragmatic layer of the calcified pericardium was not removed, because of deep penetration of the calcification inside the myocardium of the inferior right and left ventricles. Histology confirmed the tuberculous cause. Chronic calcific pericarditis is an uncommon form of pericardial inflammation. The cause is idiopathic in most cases; tuberculosis is the second most common cause of this syndrome. Pericardial calcifications occur in nearly half the people affected by chronic pericarditis and are often indicative of infective origin. Early pericardiectomy is strongly encouraged in patients suspected of having tuberculous pericarditis with massive calcification, before signs of cardiac tamponade occur.
Chromogranin A is an acidic protein present in secretory granules of neuroendocrine cells. In plasma, chromogranin A is an important marker of neuroendocrine tumours. Chromogranin A measurement has gained interest in cardiovascular disease, because increased plasma concentrations are associated with risk of clinical deterioration and death in patients with acute coronary syndromes or chronic heart failure. Cardiac chromogranin A is stored in atrial granules with cardiac natriuretic peptides—the principal cardiac hormones associated with systemic homoeostasis of water and blood pressure. Expression of cardiac chromogranin A is decreased in patients treated with mechanical assist device therapy, which parallels findings on B-type natriuretic peptide mRNA expression and concomitant plasma concentrations.1
Support for a cardiovascular role for chromogranin A comes from mice deficient in chromogranin A gene expression, because they display a hypertensive phenotype that can be fully reversed by infusion with the chromogranin A fragment catestatin.2One proposed explanation for this is that mice deficient in chromogranin A have increased catecholamine release, which is a known mechanism in essential hypertension. The first observation of chromogranin A in myocardial infarction was reported by Omland and colleagues in 2003.3 Plasma concentrations of chromogranin A were measured in 119 patients 3 days after onset of symptoms. Increased plasma chromogranin A concentrations were associated with an increased risk of death, but the association disappeared when the results were adjusted for patient age. In a later study from the same researchers,4plasma chromogranin A concentrations were found to be predictive of patient outcomes following myocardial infarction after multivariable analyses that included patient age, diabetes, and sex. The largest study so far on chromogranin A in acute coronary syndromes included 1268 patients with a follow-up of 7·5 years.5 Basal chromogranin A concentrations in plasma were strongly associated with long-term mortality, admissions to hospital for heart failure, and recurrent myocardial infarction, with hazard ratios between 1·27 (95% CI 1·10—1·47) and 1·57 (95% CI 1·44—1·70). The association was maintained even after the results were adjusted for conventional risk markers.
Chronic heart failure is characterised by pronounced activation of the neuroendocrine system and adrenal noradrenaline release; chromogranin A could be a useful clinical marker in this syndrome.6 So far, the largest study of plasma chromogranin A measurement in chronic heart failure is the GISSI-Heart Failure trial.7 The study included 1233 patients with stable heart failure and followed them up for 4 years. In univariable analysis, increased chromogranin A plasma concentrations were associated with all-cause mortality, with hazard ratios between 1·58 (95% CI 1·17—2·11) and 2·35 (95% CI 1·78—3·10). However, after adjustment for known risk factors of mortality the association was lost. Thus, this clinically well characterised study concluded that chromogranin A measurement does not seem to be useful in the assessment of mortality risk in stable chronic heart failure beyond what physical examination, routine biochemical analyses, and cardiac natriuretic peptide measurement already offer. Since this study, two small investigations have been reported on chromogranin A as a biomarker in heart failure.8, 9 Both suggest that chromogranin A measurement adds independent prognostic information beyond B-type natriuretic peptide or N-terminal pro-B-type natriuretic peptide measurement.
Measurement of plasma chromogranin A is a complex matter. Chromogranin A is a protein that contains many dibasic aminoacid motifs prone to endoproteolytical cleavage. The cellular processing of chromogranin A encompasses a plethora of fragments from the primary precursor, some of which are proposed to have independent hormonal activity (figure). However, no specific receptor-mediated mechanisms have been identified for the fragments. The primary structure of the peptide fragments also challenges the idea that they act as soluble hormones in plasma. One way around the troublesome processing of chromogranin A could be to use a processing-independent assay for measurement. By production of a uniform peptide fragment for standard measurement by epitope-specific radioimmunoassay (or other types of immunoassays), the assay can be correctly calibrated and can measure the total sum of chromogranin A translational products irrespective of its variable and poorly characterised cellular processing.10 A processing-independent assay has the general advantage of storage stability of plasma samples, since they need treatment with trypsin or another suitable endoprotease to release the measured ligand. For now, we conclude that the present studies should be interpreted with caution, because plasma chromogranin A is not a uniform analyte, and the assays used so far measure different—and often unknown—epitopes within the primary protein structure.
1 Wohlschlaeger J, von Winterfeld M, Milting H, et al. Decreased myocardial chromogranin A expression and colocalization with brain natriuretic peptide during reverse cardiac remodeling after ventricular unloading. J Heart Lung Transplant 2008;27: 442-449. CrossRef | PubMed
7 Røsjø H, Masson S, Latini Rfor the GISSI-HF Investigators. Prognostic value of chromogranin A in chronic heart failure: data from the GISSI-Heart Failure trial. Eur J Heart Fail 2010; 12: 549-556. CrossRef | PubMed
8 Dieplinger B, Gegenhuber A, Kaar G, Poelz W, Haltmayer M, Mueller T. Prognostic value of established and novel biomarkers in patients with shortness of breath attending an emergency department. Clin Biochem 2010; 43: 714-719.CrossRef | PubMed
Pulmonary hypertension is one of the leading causes of morbidity and mortality in patients with haemolytic disorders and is a frequent finding in echocardiographic screening of patients with β thalassaemia. Substantial progress has been made in understanding of the multifactorial pathophysiology of pulmonary hypertension in β thalassaemia. Haemolysis, reduced nitric oxide bioavailability, iron overload, and hypercoagulopathy are among the main pathogenetic mechanisms. Various disease-directed therapeutic methods, such as transfusion, chelation, and splenectomy, have important roles in the development of pulmonary hypertension in β thalassaemia. Studies investigating the prevalence of pulmonary hypertension in β thalassaemia are mostly based on echocardiographic findings, and are thus limited by the scarcity of information derived from right heart catheterisation. Invasive pulmonary haemodynamic data are needed to clarify the true prevalence of pulmonary hypertension in β thalassaemia, to better understand the underlying pathophysiology and risk factors, and to define the optimum therapy for this devastating complication.
Hypertension leads to reduced cerebral blood flow (CBF), which is associated with cognitive decline. However, aggressive blood pressure (BP) reduction in the elderly may produce cerebral hypoperfusion, resulting in falls and possibly stroke. In a proof-of-concept study, investigators recruited 37 primary-care patients aged 70 with uncontrolled clinical hypertension (defined as a systolic BP of >150 mm Hg as averaged from the second and third of 3 sitting measurements) while taking 1 antihypertensive medication. Patients were randomized to receive protocol-defined antihypertensive treatment to a target BP lower than either 130/80 mm Hg (intensive) or 140/85 mm Hg (usual). Magnetic resonance imaging to measure CBF and 24-hour ambulatory BP monitoring were performed at baseline and after 12 weeks of treatment.
At baseline, mean BP and mean CBF did not differ significantly between the two groups, and CBF did not correlate with any BP measure (clinical, ambulatory, aortic, systolic, or diastolic). At 12 weeks, mean clinical BP fell significantly from baseline in both groups; however, the reduction was significantly greater in the intensive group than in the usual group (26/17 vs. 15/5 mm Hg). Mean CBF did not change significantly from baseline in the usual group but increased significantly in the intensive-treatment group, regardless of baseline CBF. In both groups, the change in CBF correlated significantly with change in systolic BP.
Comment: In this small study, intensive blood-pressure treatment (targeted to <130/80 mm Hg) increased cerebral blood flow in elderly patients with hypertension. Whether increasing CBF by aggressive BP reduction slows cognitive decline or decreases cognitive impairment and — possibly — dementia compared with current, more conservative BP targets remains unclear. The latest revision of the National Heart, Lung, and Blood Institute‘s Joint National Committee guidelines is eagerly awaited and should shed light on BP goals in the elderly.
Source: Journal Watch Cardiology
Drinking a cup of beetroot juice can lower blood pressure, researchers say.
Most marked after three to six hours, the effect was detectable a day later.
Scientists say the nitrate in beetroot widens blood vessels to aid flow. And many people with angina use a nitrate drug to ease their symptoms.
The researchers, from Barts and The London School of Medicine and Dentistry, who have been studying beetroot’s blood pressure lowering effects for years, say more work is still needed.
And they warn there could be one unexpected consequence of drinking beetroot juice – it can turn your urine pink.
Nitrate is found naturally in soil, where it is taken in by vegetables through the roots to help them grow.
High blood pressure
- Left untreated, high blood pressure increases your risk of a heart attack or stroke
- Blood pressure is recorded as two figures – systolic, when the heart pumps blood out, and diastolic, when the heart rests
- You are said to have high blood pressure if readings on separate occasions consistently show your blood pressure to be 140/90mmHg or higher
- A blood pressure reading below 130/80mmHg is normal
Researcher Dr Amrita Ahluwalia said: “We were surprised by how little nitrate was needed to see such a large effect.
“Our hope is that increasing one’s intake of vegetables with a high dietary nitrate content, such as green leafy vegetables or beetroot, might be a lifestyle approach that one could easily employ to improve cardiovascular health.”
Prof Peter Weissberg, medical director at the British Heart Foundation, which funded the research, said: “It supports current advice that we should all be eating plenty of green veg.
“But we need larger studies in patients to determine if nitrate-rich vegetables are effective at lowering blood pressure over the long term.”
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In an interview on his 115th birthday, Mr Kimura said he was not sure why he was able to live so long.
“Maybe it’s all thanks to the sun above me,” he said. “I am always looking up towards the sky, that is how I am.”
Journalist Kanoko Matsuyama of Bloomberg News met Mr Kimura at his home last year.
“He said his secret to his longevity was eating light to live long,” Ms Matsuyama told the BBC.
“At the same time, his main carer and grand-daughter-in-law, Aiko, said his positivity helped him to live so long.”
She is already considered the world’s oldest living woman.
Objective To develop and validate a risk algorithm (QStroke) to estimate risk of stroke or transient ischaemic attack in patients without prior stroke or transient ischaemic attack at baseline; to compare (a) QStroke with CHADS2 and CHA2DS2VASc scores in patients with atrial fibrillation and (b) the performance of QStroke with the Framingham stroke score in the full population free of stroke or transient ischaemic attack.
Design Prospective open cohort study using routinely collected data from general practice during the study period 1 January 1998 to 1 August 2012.
Setting 451 general practices in England and Wales contributing to the national QResearch database to develop the algorithm and 225 different QResearch practices to validate the algorithm.
Participants 3.5 million patients aged 25-84 years with 24.8 million person years in the derivation cohort who experienced 77 578 stroke events. For the validation cohort, we identified 1.9 million patients aged 25-84 years with 12.7 million person years who experienced 38 404 stroke events. We excluded patients with a prior diagnosis of stroke or transient ischaemic attack and those prescribed oral anticoagulants at study entry.
Main outcome measures Incident diagnosis of stroke or transient ischaemic attack recorded in general practice records or linked death certificates during follow-up.
Risk factors Self assigned ethnicity, age, sex, smoking status, systolic blood pressure, ratio of total serum cholesterol to high density lipoprotein cholesterol concentrations, body mass index, family history of coronary heart disease in first degree relative under 60 years, Townsend deprivation score, treated hypertension, type 1 diabetes, type 2 diabetes, renal disease, rheumatoid arthritis, coronary heart disease, congestive cardiac failure, valvular heart disease, and atrial fibrillation
Results The QStroke algorithm explained 57% of the variation in women and 55% in men without a prior stroke. The D statistic for QStroke was 2.4 in women and 2.3 in men. QStroke had improved performance on all measures of discrimination and calibration compared with the Framingham score in patients without a prior stroke. Among patients with atrial fibrillation, levels of discrimination were lower, but QStroke had some improved performance on all measures of discrimination compared with CHADS2 and CHA2DS2VASc.
Conclusion QStroke provides a valid measure of absolute stroke risk in the general population of patients free of stroke or transient ischaemic attack as shown by its performance in a separate validation cohort. QStroke also shows some improvement on current risk scoring methods, CHADS2 and CHA2DS2VASc, for the subset of patients with atrial fibrillation for whom anticoagulation may be required. Further research is needed to evaluate the cost effectiveness of using these algorithms in primary care.
What is already known on this topic
- Methods to identify patients at high or low risk of stroke are needed to identify patients for whom interventions may be required, especially those with atrial fibrillation for whom anticoagulation might be needed
- Current methods for risk scoring, such as CHADS2 and CHA2DS2VASc, are not based on a statistical model, do not include many established risk factors, nor provide absolute risk estimates of stroke
- We have developed a new algorithm to quantify absolute risk of primary stroke which includes established risk factors and which is designed to work with the QRISK2 cardiovascular disease algorithm
- QStroke provides a valid measure of absolute stroke risk in the general population of patients free of stroke or transient ischaemic attack as shown by its performance in a separate validation cohort
- QStroke shows some improvement on current risk scoring methods, CHADS2and CHA2DS2VASc, for the subset of patients with atrial fibrillation for whom anticoagulation may be required
- Further research is needed to evaluate the clinical outcomes and cost effectiveness of using these algorithms in primary care
What this study adds
C-reactive protein (CRP), an acute phase reactant and marker of inflammation, has been shown to be associated with CRP genetic variants and incident hypertension, but it is unclear whether this link is causal. We therefore conducted a prospective, nested case–control study to examine the relationship between single-nucleotide polymorphisms (SNPs) within the CRP gene, circulating CRP levels and the development of hypertension. Plasma CRP levels and the genotypes of eight SNPs were determined in 2000 unrelated Shanghai residents, including 908 hypertensive individuals and 1092 normotensive individuals. Among the 1092 normotensives, 968 subjects were followed up for 2 years, during which 71 developed hypertension. Plasma CRP levels were independently associated with the development of hypertension in the follow-up study (odds ratio per quartile=1.64; 95% confidence interval: 1.18–2.26; P<0.001). The minor alleles of rs1130864 (P<0.001) and rs3093059 (P<0.001) were significantly associated with elevated CRP levels, and the minor alleles of rs1205, rs1800947 and rs2246469 (all P<0.001) were associated with decreased CRP levels. A haplotype-based analysis strengthened the results of single-locus analysis. However, none of the SNPs or haplotypes was significantly associated with blood pressure, incident hypertension or changes between baseline and follow-up blood pressure levels. Taken together, our findings demonstrated that plasma CRP levels were substantially associated with common genetic variants in the CRP gene and could predict the development of hypertension. However, the relationship between genotype and CRP levels was not associated with a change in hypertension risk.
Source: Hypertension Research/nature.
A 31-year-old obese male presented to the emergency department with symptoms and signs suggestive of a viral upper respiratory tract illness with a background of low exercise tolerance. Rib notching was identified on plain film chest radiography and subsequent CT of the thorax identified a moderately tight 2-mm juxta-ductal co-arctation of the aorta with multiple enlarged chest wall collaterals. The patient underwent a two-stage percutaneous procedure involving stent insertion and angioplasty up to 16 mm with significant improvement in exercise capacity and a modest reduction in blood pressure.
Incidental detection of rib notching on plain film radiography led to a diagnosis of co-arctation of the aorta in a male patient. Subsequent endovascular intervention resulted in improvements in the patient’s exercise capacity and energy levels and prevented the development of disastrous complications such as aortic dissection and cardiac failure.
Estimating the pretest probability of the presence of co-arctation of the aorta is difficult when non-specific symptoms such as lack of energy and low exercise capacity are found on clinical assessment. Radio-femoral delay is the clinical sign classically associated with co-arctation of the aorta, but in the present case the trigger was rib notching found on chest radiography.
This case is important as co-arctation can be missed during postnatal screening or develop late. Clinicians and radiologists therefore need to be aware of rib notching.
A 31-year-old obese male presented to the emergency department with shortness of breath, productive cough, chest pain, nausea and vomiting over a 4-day period. The cough was productive of green sputum. The chest pain was sharp, worst posteriorly and brought on by coughing but not on deep inspiration. His breathlessness did not limit his daily functioning, although a subjective background of lifelong reduced exercise tolerance was noted. Significantly, three family contacts had symptoms of viral upper respiratory tract infection over 2 weeks prior to presentation. There was no recent travel history. There was a chronic history of reduced exercise tolerance, intermittent headaches, leg cramps on exertion and a childhood heart murmur, but none of these were considered significant enough to require further investigation. There was no history of hypertension or diabetes. Family history was positive for ischaemic heart disease in his mother. He was on no regular medications. He was employed as an IT worker with a background in nursing, was married with three young children, was a non-smoker and consumed two to three standard drinks of alcohol per week.
On examination his blood pressure was 150/90 mm Hg, pulse was 90 bpm with a regular rhythm, respiratory rate was 19/min and temperature was 36.9°C. Cardiovascular examination revealed impalpable femoral pulses, a grade 1/6 systolic murmur and soft, non-tender calves. Respiratory examination revealed chest wall tenderness on palpation manoeuvres and right lower zone crepitations on auscultation.
These clinical features were most in keeping with an acute upper respiratory tract infection.
Initial investigations included laboratory tests (cell counts and troponin), a 12-lead ECG and plain film chest radiography. Blood investigations were negative except for an elevated white cell count consistent with an acute infection. The 12-lead ECG revealed T-wave inversions in leads V4–V6, unchanged from a previous ECG.
The chest film revealed rib notching of the under surfaces of mid and upper-thoracic ribs), a cardiothoracic ratio at the upper limit of normal and bilateral peribronchial cuffing in the lower zones consistent with bronchitis. The presence of borderline cardiomegaly and rib notching raised the possibility of aortic co-arctation or chronic anaemia.
Cardiovascular MRI revealed an unrestricted bicuspid aortic valve and left aortic arch with normal branching pattern. There was enlargement of the right brachiocephalic trunk, left subclavian artery and internal mammary arteries with large intercostal vessels collateralising the distal aorta. Mild tubular hypoplasia of the aortic arch was also noted.
The differential diagnosis of rib notching includes vascular and non-vascular causes. Vascular causes are due to enlarged collateral intercostal vessels to the distal aorta, which subject adjacent ribs to greater pressure than usual, resulting in bony erosion. Implicated vessels can be arterial as in aortic co-arctation and Takayasu’s arteritis, venous as in superior vena cava obstruction or arteriovenous as seen in arteriovenous fistulae. Non-vascular causes of rib notching include neurofibromatosis, intercostal neuromas and pseudo-rib notching where irregular cortical thickening may occur in the presence of tuberous sclerosis and hyperparathyroidism. Degrees of rib notching on chest radiography may also be of no clinical significance.
Treatment, outcome and follow-up
Preprocedural imaging consisted of cardiovascular MRI, cardiac CT angiogram and transthoracic echocardiogram. The patient underwent an uncomplicated endovascular aortic stent graft with left brachial artery and right femoral artery puncture with a 4×4 mm balloon angioplasty following an intravenous heparin bolus of 5000 IU. A Cheatham stent was deployed up to 10 mm at the level of the co-arctation and 16 mm distal to the co-arctation site. Six months after this procedure the patient reported improvement in exercise tolerance without chest pain, palpitations or leg cramps. His blood pressure was 135/80 mm Hg, slightly reduced compared with initial presentation (150/90 mm Hg) and femoral pulses were palpable bilaterally. CT angiography of the aorta revealed a patent stent without evidence of displacement or narrowing.
Twelve months after the initial procedure the patient underwent an uncomplicated percutaneous transluminal angioplasty of the thoracic stent up to 18 mm. Nine months after the angioplasty he reported further improvements in exercise capacity with no recurrence of chest pain or leg cramps. His blood pressure was 130/80 mm Hg. Echocardiography revealed normal left ventricular function with residual mild left ventricular hypertrophy. Follow-up management consisted of cardiovascular risk factor optimisation including caloric intake reduction to accompany increases in exercise as well as close monitoring of blood pressure. The patient was well at the time of writing, 32 months after the angioplasty.
Co-arctation of the aorta is the sixth most common congenital heart condition in Australia, with 92 cases recorded in 2003 at a rate of 3.6 per 10 000 live births.1 Diagnosis in adulthood is rare and has been associated with high mortality. Of those surviving past early childhood, historical data indicate 25% die before age 20, 50% by age 32, 75% by age 46 and 90% by 58 years.2 The most common cause of death was congestive heart failure, followed by aortic rupture, bacterial endocarditis and intracranial haemorrhage.2
Survival depends on the development of a collateral blood supply from the subclavian arteries (preco-arctation) to the aorta distal to the co-arctation via anastomoses with the intercostal arteries via three pathways: (1) the scapular pathway, including the transverse scapular and transverse cervical arteries originating from the thyrocervical trunk as well as the subscapular artery arising from the axillary artery; (2) the external thoracic pathway, including thoracic branches from the axillary artery; and (3) the internal mammary arteries3 (figure 4). Collateralisation is evidenced on chest x-ray as rib notching, which has been long associated with co-arctation of the aorta. The first three and last two ribs are typically spared due to their blood supply arising from branches unaffected by the co-arctation.
The sensitivity and specificity of rib notching for co-arctation of the aorta have not been defined. The first parameters concerning the utility of rib notching come from a case series of 43 patients with co-arctation of the aorta diagnosed at autopsy aged 2 years or greater from 1946.6 Some 75% of these 43 subjects had recognisable rib notching, giving a false negative rate of 25%. More recently, signs of a collateral circulation (rib notching and/or a visible internal thoracic artery) were seen in 26/38 patients with co-arctation of the aorta (68%, indicating a false negative rate of 32%)7 in one study, rib notching was seen in 39/61 patients (64%, false negative rate of 36%) in another8 and there is also case report evidence of co-arctation of the aorta without rib notching.9 These reports of false negative results of rib notching demonstrate limits to its sensitivity, but there are also reports that rib notching has limited specificity for co-arctation of the aorta despite a lack of numerical data. Rib notching has been visualised in the presence of other cardiovascular pathologies,3 non-vascular pathology4 and in up to 19% of healthy individuals10 (so-called pseudo rib notching).
There are also no reports on the sensitivity and/or specificity of radio-femoral delay, the classic examination sign associated with co-arctation of the aorta. Assessment for radio-femoral delay requires patients to uncover their groin area which may be a disincentive for clinicians in busy settings; additionally, locating femoral pulses can be difficult particularly in obese patients.11
An anecdotally reported alternative to radio-femoral delay involves comparing upper and lower limb systolic blood pressure,11 seeking a differential of at least 20 mm Hg.9 12,–,16 Sensitivity and specificity for co-arctation of the aorta have not been calculated for this technique either, and its specificity is likely to be limited by the rarity of adult co-arctation of the aorta, especially with the comparatively high prevalence of peripheral arterial disease which can alter the ankle–brachial pressure index.17
Other signs which may aid the detection of co-arctation of the aorta include comparison of capillary refill times and temperature between the upper and lower limb extremities.18
Despite the uncertain relative utility of these techniques, it is important to be aware that each can be associated with co-arctation of the aorta and may warrant focused assessment and further investigation.
- ▶ As co-arctation of the aorta can be missed during or develop after screening, clinicians and radiologists need to be aware of rib notching.
- ▶ Co-arctation of the aorta may present without hypertension and with non-specific symptoms of headache, low exercise capacity and intermittent leg cramps, which may not be considered significant enough for further investigation.
- ▶ Rib notching may be seen in co-arctation of the aorta due to enlarged collateral intercostal arteries and while not specific, mandates the consideration of co-arctation.
- ▶ Measurement of differences in lower limb and brachial arterial pressure is a reasonable and simple alternative to femoral pulse palpation but may be confounded by peripheral arterial disease.
- ▶ Capillary refill and temperature differences between the upper and lower limb extremities may also indicate co-arctation of the aorta.
Dr Jenny Ho (Central City Medical Centre, Perth, Western Australia) is thanked for her support.
- Competing interests None.
- Patient consent Obtained.
Australian Institute of Health and Welfare 2011. In: Cardiovascular disease: Australian facts 2011. Cardiovascular disease series. Cat. no. CVD 53. Canberra: AIHW 2011.
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