Computed Tomography: Coronary Angiography
Coronary CT angiography (CCTA) noninvasively assesses patency of the coronary lumen, the arterial wall, calcified and noncalcified plaques, and ventricular function
In addition to many single-center studies, 3 multicenter trials evaluated the diagnostic use of 64-slice CCTA and reported sensitivities for detecting a 50% stenosis from 85% to 99%, with negative predictive values from 83% to 99% .
It is not known, however, whether CCTA can be used as a prognostic tool, independent of CACS ( Coronary artery Calcium Score) and clinical risk models, to stratify asymptomatic patients and predict future cardiac events.
In patients who had suspected but undocumented CAD, Russo et al evaluated the incremental prognostic value of CCTA against both a traditional clinical-risk model and calcium scoring.
While CACS again had significant incremental prognostic value compared with a baseline clinical-risk model, CCTA provided an additional incremental prognostic value, compared with a baseline clinical-risk model plus CACS.
The presence of non calcified or mixed plaques, regardless of lesion severity, was found to be the strongest predictor of events (P<.0001) as a potential marker of plaque vulnerability.
Using CCTA in asymptomatic patients remains controversial, primarily because of the higher radiation dose, added cost, and use of nephrotoxic contrast, but it has the potential to identify useful data beyond what is derived from CACS.
As detailed in the 2010 ACCF/AHA Guideline for Assessment of Cardiovascular Risk ,
CCTA is not recommended for cardiovascular risk assessment in asymptomatic adults .
G Mohan.
CORONARY ANGIOGRAPHY-CCTA.
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gmohan
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CORONARY ANGIOGRAPHY-CCTA.
Last edited by gmohan on 19 Sep 2016 01:21, edited 3 times in total.
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Badri
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Re: CORONARY ANGIOGRAPHY-CCTA.
One of the problems with any angiography is that the contrast can affect kidney function. A friend of mine who had a heart problem needed an angiogram before a decision could be made about surgery. Unfortunately he was also diabetic and had a below normal kidney function. He was refused an angiogram and was told that his kidney may fail with the contrast and he may require dialysis. The poor man was petrified of dialysis but did not realise how serious his heart problem was. Within a year of this dilemma he had an arrest and died on the way to hospital.
Now my question is how would you go about investigating someone with a poor renal function with a cardiac problem that requires an angiogram (and contrast).
Now my question is how would you go about investigating someone with a poor renal function with a cardiac problem that requires an angiogram (and contrast).
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gmohan
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Re: CORONARY ANGIOGRAPHY-CCTA.
Badri,
Allow me to address your question ,specifically on THE TWO issues separately , and the both issues Combined.
Firstly a patient with REDUCED RENAL FUNCTION .
Secondly a patient with DIABETES MELLITUS.
Thirdly a patient with BOTH REDUCED RENAL FUNCTION AND DIABETES MELLITUS.
To follow.
Allow me to address your question ,specifically on THE TWO issues separately , and the both issues Combined.
Firstly a patient with REDUCED RENAL FUNCTION .
Secondly a patient with DIABETES MELLITUS.
Thirdly a patient with BOTH REDUCED RENAL FUNCTION AND DIABETES MELLITUS.
To follow.
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uamohammed
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Re: CORONARY ANGIOGRAPHY-CCTA.
Hi Mohan and Badri
The risk of contrast medium causing nephropathy is there whether we use plain angiography or CT angiography. I just want to know from Mohan if we use MRI instead of CT for angiography is it not better as MRI has no radiation risk and we use different contrast media, that is gadolinium which causes nephrogenic systemic fibrosis the risk of which I understand is very remote.
We are all worried about nephropathy after a contrast medium usage. But though not that much alarming as nephropathy, we should not forget that a large dose of iodine injected may convert a borderline case of hyperthyroidism into a florid one resulting in severe cardiac arrhythmia and failure. Therefore when we send patients for imaging using contrast media containing iodine, in addition to RFT we should investigate thyroid function test also.
UA Mohammed
The risk of contrast medium causing nephropathy is there whether we use plain angiography or CT angiography. I just want to know from Mohan if we use MRI instead of CT for angiography is it not better as MRI has no radiation risk and we use different contrast media, that is gadolinium which causes nephrogenic systemic fibrosis the risk of which I understand is very remote.
We are all worried about nephropathy after a contrast medium usage. But though not that much alarming as nephropathy, we should not forget that a large dose of iodine injected may convert a borderline case of hyperthyroidism into a florid one resulting in severe cardiac arrhythmia and failure. Therefore when we send patients for imaging using contrast media containing iodine, in addition to RFT we should investigate thyroid function test also.
UA Mohammed
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gmohan
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IV CONTRAST MEDIA IN DIABETES ,AND WITH METFORMIN
METFORMIN ,DIABETES MELITUS and IV contrast Media
Last updated: 23 May 2016-AMERICAN COLLEGE OF RADIOLOGY.
Metformin is a biguanide oral anti-hyperglycemic agent used primarily, but not exclusively, to treat patients with non-insulin-dependent diabetes mellitus . It is available as a generic drug as well as in proprietary formulations, alone and in combination with other drugs The drug was approved in the United States in December of 1994 for use as monotherapy or combination therapy in patients with non-insulin-dependent diabetes mellitus whose hyperglycemia is not controlled by diet or sulfonylurea therapy alone.
Metformin is thought to act by decreasing hepatic glucose production and enhancing peripheral glucose uptake as a result of increased sensitivity of peripheral tissues to insulin. Only rarely does it cause hypoglycemia.
The most significant adverse effect of metformin therapy is the potential for the development of metformin-associated lactic acidosis in the susceptible patient.
This condition is estimated to occur at a rate of 0 to 0.084 cases per 1,000 patient years. Patient mortality in reported cases is about 50%. However, in almost all reported cases, lactic acidosis occurred because one or more patient-associated contraindications for the drug were overlooked. In one extensive 13-year retrospective study of patients in Sweden, 16 cases were found and all patients had several comorbid factors, most often cardiovascular or renal disease. There are no documented cases of metformin-associated lactic acidosis in properly selected patients.
Metformin is excreted unchanged by the kidneys, probably by both glomerular filtration and tubular excretion. The renal route eliminates approximately 90% of the absorbed drug within the first 24 hours. Metformin seems to cause increased lactic acid production by the intestines.
Any factors that decrease metformin excretion or increase blood lactate levels are important risk factors for lactic acidosis. Renal insufficiency, then, is a major consideration for radiologists.
Also, factors that depress the ability to metabolize lactate, such as liver dysfunction or alcohol abuse, or that increase lactate production by increasing anaerobic metabolism (e.g., cardiac failure, cardiac or peripheral muscle ischemia, or severe infection) are contraindications to the use of metformin.
Iodinated X-ray contrast media are not an independent risk factor for patients taking metformin but are a concern only if post-contrast acute kidney injury (AKI) should develop. Please refer to the chapter on Postcontrast Acute Kidney Injury and Contrast-Induced Nephropathy in Adults for information about the risk of these events.
The metformin package inserts approved by the U.S. Food and Drug Administration state that metformin should be withheld temporarily for patients undergoing radiological studies using IV iodinated contrast media. If acute kidney injury were to be caused by the iodinated contrast media, an accumulation of metformin could occur, with resultant lactate accumulation.
Management
The management of patients taking metformin should be guided by the following:
1. Patients taking metformin are not at higher risk than other patients for post-contrast acute kidney injury.
2. Iodinated contrast is a potential concern for furthering renal damage in patients with acute kidney injury, and in patients with severe chronic kidney disease (stage IV or stage V).
3. There have been no reports of lactic acidosis following intravenous iodinated contrast medium administration in patients properly selected for metformin administration.
The Committee recommends that patients taking metformin be classified into one of two categories based on the patient’s renal function (as measured by eGFR).
Category I
In patients with no evidence of AKI and with eGFR ≥30 mL / min/1.73m2, there is no need to discontinue metformin either prior to or following the intravenous administration of iodinated contrast media, nor is there an obligatory need to reassess the patient’s renal function following the test or procedure.
Category II
In patients taking metformin who are known to have acute kidney injury or severe chronic kidney disease (stage IV or stage V; i.e., eGFR< 30), or are undergoing arterial catheter studies that might result in emboli (atheromatous or other) to the renal arteries, metformin should be temporarily discontinued at the time of or prior to the procedure, and withheld for 48 hours subsequent to the procedure and reinstituted only after renal function has been re-evaluated and found to be normal.
Metformin and Gadolinium
It is not necessary to discontinue metformin prior to contrast medium administration when the amount of gadolinium-based contrast material administered is in the usual dose range of 0.1 to 0.3 mmol per kg of body weight.
G Mohan
Last updated: 23 May 2016-AMERICAN COLLEGE OF RADIOLOGY.
Metformin is a biguanide oral anti-hyperglycemic agent used primarily, but not exclusively, to treat patients with non-insulin-dependent diabetes mellitus . It is available as a generic drug as well as in proprietary formulations, alone and in combination with other drugs The drug was approved in the United States in December of 1994 for use as monotherapy or combination therapy in patients with non-insulin-dependent diabetes mellitus whose hyperglycemia is not controlled by diet or sulfonylurea therapy alone.
Metformin is thought to act by decreasing hepatic glucose production and enhancing peripheral glucose uptake as a result of increased sensitivity of peripheral tissues to insulin. Only rarely does it cause hypoglycemia.
The most significant adverse effect of metformin therapy is the potential for the development of metformin-associated lactic acidosis in the susceptible patient.
This condition is estimated to occur at a rate of 0 to 0.084 cases per 1,000 patient years. Patient mortality in reported cases is about 50%. However, in almost all reported cases, lactic acidosis occurred because one or more patient-associated contraindications for the drug were overlooked. In one extensive 13-year retrospective study of patients in Sweden, 16 cases were found and all patients had several comorbid factors, most often cardiovascular or renal disease. There are no documented cases of metformin-associated lactic acidosis in properly selected patients.
Metformin is excreted unchanged by the kidneys, probably by both glomerular filtration and tubular excretion. The renal route eliminates approximately 90% of the absorbed drug within the first 24 hours. Metformin seems to cause increased lactic acid production by the intestines.
Any factors that decrease metformin excretion or increase blood lactate levels are important risk factors for lactic acidosis. Renal insufficiency, then, is a major consideration for radiologists.
Also, factors that depress the ability to metabolize lactate, such as liver dysfunction or alcohol abuse, or that increase lactate production by increasing anaerobic metabolism (e.g., cardiac failure, cardiac or peripheral muscle ischemia, or severe infection) are contraindications to the use of metformin.
Iodinated X-ray contrast media are not an independent risk factor for patients taking metformin but are a concern only if post-contrast acute kidney injury (AKI) should develop. Please refer to the chapter on Postcontrast Acute Kidney Injury and Contrast-Induced Nephropathy in Adults for information about the risk of these events.
The metformin package inserts approved by the U.S. Food and Drug Administration state that metformin should be withheld temporarily for patients undergoing radiological studies using IV iodinated contrast media. If acute kidney injury were to be caused by the iodinated contrast media, an accumulation of metformin could occur, with resultant lactate accumulation.
Management
The management of patients taking metformin should be guided by the following:
1. Patients taking metformin are not at higher risk than other patients for post-contrast acute kidney injury.
2. Iodinated contrast is a potential concern for furthering renal damage in patients with acute kidney injury, and in patients with severe chronic kidney disease (stage IV or stage V).
3. There have been no reports of lactic acidosis following intravenous iodinated contrast medium administration in patients properly selected for metformin administration.
The Committee recommends that patients taking metformin be classified into one of two categories based on the patient’s renal function (as measured by eGFR).
Category I
In patients with no evidence of AKI and with eGFR ≥30 mL / min/1.73m2, there is no need to discontinue metformin either prior to or following the intravenous administration of iodinated contrast media, nor is there an obligatory need to reassess the patient’s renal function following the test or procedure.
Category II
In patients taking metformin who are known to have acute kidney injury or severe chronic kidney disease (stage IV or stage V; i.e., eGFR< 30), or are undergoing arterial catheter studies that might result in emboli (atheromatous or other) to the renal arteries, metformin should be temporarily discontinued at the time of or prior to the procedure, and withheld for 48 hours subsequent to the procedure and reinstituted only after renal function has been re-evaluated and found to be normal.
Metformin and Gadolinium
It is not necessary to discontinue metformin prior to contrast medium administration when the amount of gadolinium-based contrast material administered is in the usual dose range of 0.1 to 0.3 mmol per kg of body weight.
G Mohan
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gmohan
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PREVENTION OF CONTRAST INDUCED ACUTE KIDNEY INJURY in ADULTS
Prevention of Contrast Induced Acute Kidney Injury (CI-AKI) In Adult Patients
The Renal Association GB,
British Cardiovascular Intervention Society and The Royal College of Radiologists
The use of intravascular iodinated contrast agents has continued to increase over recent years. It is recognised that there are potential risks associated with the intravascular administration of iodinated contrast agents. It is, therefore, essential
We would encourage practitioners, wherever practicable, to adopt the current trend towards reduced doses of intravenous iodinated contrast media due to the benefit of modern dual-head pumps and fast CT scanners. At the time of publishing these guidelines, investigations into the potential of low-kVp, low iodinated contrast dose CT technique, were in progress.
These guidelines address the issues associated with administering iodinated contrast agents to adult patients only. For children and neonates a paediatric radiologist should be consulted.
Rationale
Acute kidney injury following receipt of iodinated contrast (CI-AKI) has previously been referred to as contrast induced nephropathy (CIN) defined as a rise in serum creatinine by 25% or 44μmol/L from the baseline value.
It is uncommon in the general population, with an incidence of 1-2%, and occurs within 72 hours of receiving contrast media, usually recovering over the following five days.
It is important to exclude other causes of AKI as small rises in serum creatinine have been demonstrated to occur in 8-35% of patients admitted to hospital without exposure to contrast media.
Its incidence increases significantly in patients with risk factors and is associated with increased mortality.
Rationale
The risk of CI-AKI is low in patients with normal kidney function, estimated at 1–2% even in patients with diabetes.
However prior exposure to iodinated contrast media has been identified as the third most common aetiogical factor for AKI in hospital after renal hypoperfusion and nephrotoxic medication.
The risk of CI-AKI has been reported to be as high as 25% in patients with a combination of chronic kidney disease (CKD) and diabetes, cardiac failure, older age and exposure to nephrotoxic drugs.
The CI-AKI Consensus Working Panel has recommended that the risk of CI-AKI becomes clinically important with an eGFR <60 ml/min/1.73m.
Acutely ill patients with sepsis and/or hypotension are particularly vulnerable to injury following iodinated contrast exposure. There is a general consensus that the risk of CI-AKI is higher after arterial compared to venous administration of iodinated contrast media although this has not been proven convincingly.
Risk factors for patients developing CI-AKI include
chronic kidney disease (CKD) eGFR <60ml/min/1.73m2
older age (>75 years old)
cardiac failure
nephrotoxic medication
o aminoglycosides o NSAIDs
o Amphotericin B
hypovolaemia
sepsis
volume (dose) of contrast
intra-arterial administration
It should be appreciated that often a number of these risk factors will be present together in a patient, and that there is currently no validated CI-AKI risk assessment available to recommend.
The use of the estimated glomerular filtration rate (eGFR) to quantify kidney function should only be applied to patients with stable kidney function and should not be used in patients with AKI. Patients identified as at high risk
of CI-AKI may be discussed with a renal physician to assess the individual risk/benefit associated with a specific contrast procedure. In some patients the risk of CI-AKI is outweighed by the potential benefit from the contrast study.
It is recommended that these risks are explained to the patient in the context of the potential benefit of proceeding with the study. Imaging should not be delayed where the benefit of early imaging clearly outweighs the risk of waiting. [/color
This effectively concludes the Chapter on RADIOLOGY IN CARDIO VASCULAR DISEASE.
G Mohan
The Renal Association GB,
British Cardiovascular Intervention Society and The Royal College of Radiologists
The use of intravascular iodinated contrast agents has continued to increase over recent years. It is recognised that there are potential risks associated with the intravascular administration of iodinated contrast agents. It is, therefore, essential
We would encourage practitioners, wherever practicable, to adopt the current trend towards reduced doses of intravenous iodinated contrast media due to the benefit of modern dual-head pumps and fast CT scanners. At the time of publishing these guidelines, investigations into the potential of low-kVp, low iodinated contrast dose CT technique, were in progress.
These guidelines address the issues associated with administering iodinated contrast agents to adult patients only. For children and neonates a paediatric radiologist should be consulted.
Rationale
Acute kidney injury following receipt of iodinated contrast (CI-AKI) has previously been referred to as contrast induced nephropathy (CIN) defined as a rise in serum creatinine by 25% or 44μmol/L from the baseline value.
It is uncommon in the general population, with an incidence of 1-2%, and occurs within 72 hours of receiving contrast media, usually recovering over the following five days.
It is important to exclude other causes of AKI as small rises in serum creatinine have been demonstrated to occur in 8-35% of patients admitted to hospital without exposure to contrast media.
Its incidence increases significantly in patients with risk factors and is associated with increased mortality.
Rationale
The risk of CI-AKI is low in patients with normal kidney function, estimated at 1–2% even in patients with diabetes.
However prior exposure to iodinated contrast media has been identified as the third most common aetiogical factor for AKI in hospital after renal hypoperfusion and nephrotoxic medication.
The risk of CI-AKI has been reported to be as high as 25% in patients with a combination of chronic kidney disease (CKD) and diabetes, cardiac failure, older age and exposure to nephrotoxic drugs.
The CI-AKI Consensus Working Panel has recommended that the risk of CI-AKI becomes clinically important with an eGFR <60 ml/min/1.73m.
Acutely ill patients with sepsis and/or hypotension are particularly vulnerable to injury following iodinated contrast exposure. There is a general consensus that the risk of CI-AKI is higher after arterial compared to venous administration of iodinated contrast media although this has not been proven convincingly.
Risk factors for patients developing CI-AKI include
chronic kidney disease (CKD) eGFR <60ml/min/1.73m2
older age (>75 years old)
cardiac failure
nephrotoxic medication
o aminoglycosides o NSAIDs
o Amphotericin B
hypovolaemia
sepsis
volume (dose) of contrast
intra-arterial administration
It should be appreciated that often a number of these risk factors will be present together in a patient, and that there is currently no validated CI-AKI risk assessment available to recommend.
The use of the estimated glomerular filtration rate (eGFR) to quantify kidney function should only be applied to patients with stable kidney function and should not be used in patients with AKI. Patients identified as at high risk
of CI-AKI may be discussed with a renal physician to assess the individual risk/benefit associated with a specific contrast procedure. In some patients the risk of CI-AKI is outweighed by the potential benefit from the contrast study.
It is recommended that these risks are explained to the patient in the context of the potential benefit of proceeding with the study. Imaging should not be delayed where the benefit of early imaging clearly outweighs the risk of waiting. [/color
This effectively concludes the Chapter on RADIOLOGY IN CARDIO VASCULAR DISEASE.
G Mohan
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gmohan
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- Full Name: Govind Mohan
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MRI -ACS
Hello Mohammed,
Salient points raised by you re MRI.
Please access the forum article in full on MRI and its present status in Acute coronary syndromes.
Thank you.
G Mohan.
Salient points raised by you re MRI.
Please access the forum article in full on MRI and its present status in Acute coronary syndromes.
Thank you.
G Mohan.