Quiz feedback: CVRA and Managing thyroid dysfunction

In the 1990s, researchers published an algorithm for predicting risk of future cardiovascular events, based on the findings of the long running Framingham Heart Study, based in Framingham, Massachusetts. The factors used to calculate cardiovascular risk based on the Framingham risk score are; age, gender, systolic blood pressure, total cholesterol:HDL cholesterol ratio, smoking status and presence of diabetes mellitus.

Around one-fifth of respondents selected “diastolic blood pressure” as a variable in the Framingham calculation. While it is correct that blood pressure is part of the risk equation, it is the systolic reading which is used in the calculation, rather than diastolic.

To adapt the Framingham risk score for a local context, New Zealand risk charts allow for an additional 5% to be added based on ethnicity (Maori, Pacific peoples and people from the Indian subcontinent) and family history of cardiovascular disease (premature coronary heart disease or ischaemic stroke in a father or brother aged < 55 years or a mother or sister aged < 65 years).

Just under half of respondents indicated that “diabetes status” was an additional factor added to calculation of cardiovascular risk in the New Zealand context. However, diabetes is one of the classic cardiovascular risk factors that are incorporated into the original Framingham equation. Renal function and socioeconomic factors are important predictors of risk but are not currently allowed for in risk equations.

Renal function and socioeconomic factors are important predictors of risk but are not currently allowed for in risk equations (although 5% is added to the risk calculation for people with diabetes and microalbuminuria).

New Zealand Guidelines allow for an additional 5% to be added to the calculated five-year cardiovascular risk if there is a family history of premature coronary heart disease or ischaemic stroke in a first-degree relative, i.e. a father or brother aged < 55 years or a mother or sister aged < 65 years.

Obesity is recognised as a risk factor for cardiovascular disease, however, the significance of the risk is dependent on other factors such as the presence of raised blood pressure, glucose or lipid levels. Less intensive management (e.g. diet and exercise) could be considered if a patient was obese without any other risk factors.

Although not a traditional marker of cardiovascular risk, it is now increasingly recognised that chronic renal dysfunction is an independent risk factor. Measures to reduce cardiovascular risk should be considered for people with an eGFR measurement less than 60 mL/min/1.73 m².

When considered independently, elevated triglyceride levels are considered to only have a weak effect on cardiovascular risk assessment.

None of these answers are correct. There is no conclusive evidence that any of these surrogate markers should be routinely measured as part of a cardiovascular risk assessment.

There is no evidence that reducing an elevated level of lipoprotein (a) results in a reduction in the incidence of first or subsequent cardiovascular events. In addition, lipoprotein (a) levels are hard to alter clinically. Therefore widespread testing of lipoprotein (a) levels and attempts to reduce levels are neither recommended nor warranted.

Folic acid is known to lower homocysteine levels, however this does not appear to reduce cardiovascular risk. There is no evidence that homocysteine is a reliable marker of cardiovascular disease.

The evidence is inconclusive whether high sensitivity CRP (HsCRP) has a direct effect on cardiovascular risk prediction. Elevated HsCRP could indicate atherosclerosis, but levels can also be temporarily raised by inflammation. In addition, there is significant individual variation in baseline levels.

Observational studies have shown an association between low vitamin D levels and increased risk of cardiovascular events. There is also a suggestion that vitamin D has a protective effect in terms of cardiovascular risk, for patients using calcium supplements. However, the evidence is limited and not sufficient to justify widespread vitamin D supplementation or testing.

There is mixed evidence as to whether uric acid is an independent marker of cardiovascular risk. Although over one quarter of respondents selected uric acid as a marker that should be routinely measured as part of cardiovascular risk assessment, the jury is still out.

Vitamin D may be associated with reduced risk of cardiovascular disease, but the evidence is limited and not sufficient to justify widespread vitamin D supplementation or testing.

A recent meta-analysis evaluating the benefits and harms of low-dose aspirin in people with diabetes, has shown no clear benefit of aspirin in terms of reducing cardiovascular risk. Therefore routine use of aspirin in people with diabetes is not advocated.

Folic acid is used to lower homocysteine levels, however studies have failed to show that folic acid actually decreased cardiovascular events and may increase risk in some patients with high homocysteine levels at baseline. Folic acid supplementation is not recommended to lower homocysteine levels or reduce cardiovascular risk.

A pooled analysis of intervention trials found that a mean daily consumption of 40 g to 100 g of raw nuts (including peanuts) may reduce cardiovascular risk and blood lipid levels.

Just over one-third of respondents correctly identified that calcium supplementation is not thought to increase cardiovascular risk, based on limited evidence. A systematic review showed neutral effects of calcium on cardiovascular disease. While calcium probably does not increase cardiovascular risk, there is also no strong evidence that it provides any benefit.

Around one-quarter of respondents selected the first three symptoms and signs as indicating a high suspicion of thyroid dysfunction. Fatigue, hair loss and fine tremor may indicate a low suspicion of thyroid dysfunction, but they are non-specific and could be related to a number of other conditions.

Delayed reflexes indicate a high suspicion of hypothyroidism and proptosis (bulging eyes) indicates a high suspicion of hyperthyroidism.

Most respondents correctly selected the true statements about testing for thyroid dysfunction.

There is a lack of evidence to support routine screening in asymptomatic people, therefore testing for thyroid dysfunction is not recommended unless there are symptoms and signs of thyroid disease. When indicated, TSH is the most appropriate initial test to investigate thyroid dysfunction. FT4 may also be requested if the patient is pregnant or if it is suspected that they have pituitary failure.

Amiodarone causes either hyper or hypothyroidism in approximately 14-18% of treated patients, due to the high iodine content in this medicine and its direct toxic effect on the thyroid. Long-term treatment with lithium may also cause thyroid dysfunction, but hypothyroidism is more common than hyperthyroidism.

People who have had treatment with radioactive iodine therapy or surgery for hyperthyroidism are at an increased risk of hypothyroidism and should be screened with a TSH test every one or two years or if there are signs or symptoms of thyroid disease.

Monitoring of both TSH and FT4 is required for women at increased risk of thyroid dysfunction during pregnancy. TSH may be temporarily suppressed during the first trimester due to the thyroid stimulating effect of hCG. FT4 levels tend to decrease in the second half of pregnancy.

All options are correct – TSH testing is appropriate in all of these scenarios. Around one-third of respondents did not identify that TSH testing is appropriate three to four months after the target TSH level has been reached and when a different brand of levothyroxine is started.

When levothyroxine is used to treat hypothyroidism, symptoms begin to improve within two to three weeks, however it can take several months before a patient feels back to normal health. Once the target TSH has been reached for the first time, a further TSH test in three to four months is useful to ensure that the TSH is stable.

There are several brands of levothyroxine available in New Zealand. Although the levothyroxine content in the different brands is the same, the additional tablet constituents may affect absorption. Therefore TSH testing is recommended six weeks after a patient switches brands, to ensure that the same control has been achieved.

Anti-thyroid medicines (e.g. carbimazole), radioactive iodine and surgery (e.g. thyroidectomy) are the main options for the treatment of persistent hyperthyroidism. Although only selected by half of the respondents, beta-blockers such as propranolol can be part of a treatment regimen for hyperthyroidism, to control symptoms such as tremor and tachycardia.

Levothyroxine is used to treat hypothyroidism.

The majority of respondents identified the correct options for this question.

Routine screening for thyroid dysfunction in women planning a pregnancy and those who are pregnant is not recommended in New Zealand as not all people are at risk.

TSH levels can be suppressed during the first trimester of pregnancy due to the thyroid stimulating effect of hCG. Rather than increase, FT4 levels tend to slowly decrease in the second half of pregnancy.

In women taking levothyroxine, doses generally need to be increased during the first trimester of pregnancy. Dose requirements stabilise by 20 weeks and fall back to non-pregnant levels in a short time after delivery.