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CARDIO-OBSTETRICS

Cardio-obstetrics refers to a team-based approach to maternal care that includes collaboration among maternal fetal medicine, cardiology, anesthesiology, neonatology, nursing, social work, and pharmacy.

Recognizing and measuring outcomes associated with various types of maternal CVD is an important and fundamental role of cardio-obstetric programs. In a recent statement, the American Heart Association emphasized the role of cardio-obstetrics in addressing and decreasing maternal morbidity and mortality in the preconception, antepartum, and postpartum periods.

In a 2019 Practice Bulletin, the American College of Obstetricians and Gynecologists (ACOG) defined 4 risk factors related to CVD-related mortality in pregnant and postpartum patients: race/ethnicity, advanced age, hypertension, and obesity.

Cardiac Disease in Pregnancy (CARPREG II) score

The score incorporates 10 predictors of adverse cardiac events during pregnancy including prior cardiac events or arrhythmias, baseline New York Heart Association functional class, mechanical valve, ventricular dysfunction, high-risk left-sided valve disease/left ventricular outflow tract obstruction, pulmonary hypertension, coronary artery disease, high-risk aortopathy, no prior cardiac intervention, and late pregnancy assessment (defined as first antenatal visit >20 weeks)

Patients are categorized by scores of 0–1, 2, 3, 4, and >4, with higher scores associated with increased risk of maternal cardiac events.

Cardio-obstetrics teams are multidisciplinary and provide comprehensive care for women throughout the preconception, antepartum, and postpartum periods. The need for increased research collaboration regarding cardio-obstetrics has been identified, and the field of maternal cardiac care and cardio-obstetrics is evolving as an area of focus among cardiologists

The goal of the cardio-obstetrics model is to provide comprehensive maternal care. This should incorporate preconception counseling for women with pre-existing medical problems, consideration of referral versus co-management options, promotion of management guidelines to care for high-risk maternal patients, as well as multidisciplinary case conferences where complex cases can be discussed with a variety of care providers. In addition, comprehensive maternal care centers allows for colocalization of specialists across disciplines including maternal fetal medicine, cardiology, neurology, surgery, and endocrinology for mothers before, during, and after high-risk pregnancies in the same physical space

WHEN TO CREATE A SHUNT IN PULMONARY HYPERTENSION (PH)

Shunts can be created in selected cases of advanced pulmonary hypertension, in view of off-loading the right ventricle and improving cardiac output at the cost of cyanosis. Shunt creation is not without risks and remains indicated only in selected severe cases.
Observing that patients with ES have reported better survival than patients with idiopathic PAH, physicians have started to create shunts in severe idiopathic PAH to allow for right-to-left shunting. The aim is to prolong survival, postpone lung transplant, or improve quality of life at the expense of systemic arterial desaturation

Atrial septostomy has been performed as a palliative procedure for patients with refractory PAH since 1983. In patients with a failing RV and elevated right atrial pressure (RAp), pretricuspid right-to-left shunting unloads the RV and improves left ventricular preload and systemic cardiac output. It is worth mentioning that unlike adults, children with PAH seldom have elevated RAp. Atrial septostomy has the advantage of being a percutaneous procedure, either via blade septostomy or balloon dilation of the atrial septum. It has been reported that atrial septostomy improves symptoms (most notably syncope) and quality of life in adults and children with PAH.
A meta-analysis has recently been published demonstrating benefits with this intervention. It may also serve as a bridge to lung transplantation. The procedural morbidity of atrial septostomy is mainly related to uncontrolled right-to-left shunting, resulting in insufficient PBF and profound hypoxemia in patients with elevated RAp and large defects. The relative contraindications for atrial septostomy are a mean RAp > 20 mm Hg, a resting oxygen saturation < 90%, and severe RV failure. Another longer-term disadvantage is the risk of paradoxical cerebral thromboembolism. The international guidelines suggest considering atrial septostomy in patients in World Health Organization (WHO) functional Group III and Group IV with recurrent syncope on combined medical therapy.

A reversed Potts shunt is the creation of a connection between the left pulmonary artery and the descending aorta, which allows right-to-left shunting (hence the term “reversed”). It has the advantage over atrial septostomy of providing oxygenated blood to the brain and the coronary arteries and only causes desaturation of the lower body. The reversed Potts shunt relieves RV pressure overload in systole and in diastole, improves RV–pulmonary artery coupling, and improves left ventricular performance by reducing the interventricular septum left shift. It has the potential to be effective before RV failure develops. The chief concern remains the risk of operating in PAH patients who have a nonnegligible anesthetic and surgical mortality. Transcatheter procedures have been performed in some highly experienced centers, either by stenting an existing small patent ductus arteriosus, or by creating a transcatheter de novo stent–secured aortopulmonary connection, though this approach also appears to carry a high risk of severe complications. Regardless of the technique, reversed Potts shunt creation remains a high-risk procedure with a reported mortality of 12% to 30%. One of the main complications is an early acute low-output state secondary to sudden reduction in the left ventricular preload. Despite the high periprocedural mortality, long-term results are very encouraging, with prolonged survival and improvement in functional status, allowing progressive weaning from prostanoids in children. Further studies should help to understand if these favorable effects are long-lasting and further define the indications and contraindications of the procedure. As per the international guidelines, reversed Potts shunt “may be considered in patients with suprasystemic PH refractory to any medical treatment, including combined therapy presenting with WHO FC IV symptoms.

Thiamine-Responsive Acute Pulmonary Hypertension of Early Infancy (TRAPHEI)

(Source Children 2020, 7, 199)

While malnutrition-induced PH is likely a rare finding, instances of vitamin D3, vitamin C and thiamine (B1) deficiency causing PH are observed across different age groups. Recently several cases of postneonatal pulmonary hypertension are reported from India. Infantile thiamine deficiency related symptoms most commonly occur between 1 and 7 months of age. However, acute cardiac
manifestations of Shoshin beriberi are more common among young infants between 1 and 3 months of age.

Risk factors for TRAPHEI include exclusive breastfeeding by thiamine-deficient but otherwise asymptomatic mothers. Mothers who consume exclusive polished white rice that has been washed
multiple times are at the highest risk of thiamine deficiency. Young infants (1–3 months of age) exclusively breastfed are at greatest risk for developing thiamine deficiency. Thiamine deficiency has a wide range of clinical presentations, with high fatality in untreated cases and survivors usually have long-term sequelae.

The clinical presentation in patients was typical of PH exacerbated by a respiratory illness in previously healthy infants on exclusive breast feeding. These patients had severe respiratory distress, refractory hypoxemia, PH and lactic acidosis with some requiring mechanical ventilation, pulmonary vasodilators and inotropic
support. These infants had a typical history of maternal customary dietary restriction and consumption of exclusive repeatedly washed and polished white rice and wheat flour. Infants rapidly responded
to IV infusion of thiamine 100 mg over 20–30 min and showed clinical improvement over the next 2–4 h. All infants received enteral thiamine for a few weeks. After 24–48 h of thiamine, significant improvement in PH was observed in these infants. Although, sildenafil and bosentan were used in the management of these patients, these medications did not result in any significant change in clinical outcomes. Follow-up after 4 to 6 weeks of thiamine therapy showed complete resolution of this form of postneonatal pulmonary hypertension

Diagnosis of TRAPHEI can be considered if the infant at risk presents with respiratory failure and has all of the following criteria: (1) newly diagnosed pulmonary hypertension without any
pre-existing congenital heart disease or chronic pulmonary condition,
(2) metabolic acidosis with elevated lactate,
(3) no other cause for this illness including sepsis,
(4) maternal dietary history suggestive of thiamine-deficiency in an exclusively or predominantly breastfed infant and
(5) rapid response to IV thiamine challenge

Congenital heart defects in IVF/ICSI pregnancy:
(Systematic review and meta-analysis)

TO ASSESS WHETHER CONGENITAL HEART DEFECTS (CHD) OCCUR MORE OFTEN IN PREGNANCIES CONCEIVED AFTER IVF/ICSI AS COMPARED WITH THOSE CONCEIVED SPONTANEOUSLY.

Summary of evidences
The risk of CHD in IVF/ICSI pregnancies is significantly increased as compared to spontaneous conceptions by about 50%, with stable significance in most subgroup analyses.
Previous studies assessing the risk of CHD in pregnancies conceived after IVF/ICSI showed a slightly higher risk in this group as compared to spontaneous conceptions. Previous meta-analyses also showed an increased risk of all congenital malformation in IVF/ICSI infants without significant risk difference between IVF and ICSI. This may be due to the ART procedure or to several other risk factors such as the underlying infertility cause or twins pregnancies.
There is no consensus in current practice guidelines whether IVF/ICSI conception represents an indication for performing a fetal echocardiogram according to different eminent scientific societies. American Institute of Ultrasound in Medicine, America Society of Echocardiography and American Heart Association (AHA) consider IVF an indication for a detailed cardiac scan, but only AHA guideline includes IVF or ICSI among maternal indications for fetal echocardiogram with recommendation class/level of evidence of IIa/A estimating and an absolute risk of 1.1-3.3% among live births.
Overall, 25856 fetuses obtained from IVF/ICSI techniques were compared to 287995 fetuses spontaneously conceived, both in singleton and multiple pregnancies. The total CHD events were 337/25856 (1.30 %) and 1952/287995 (0.68 %) in the IVF/ICSI and spontaneous conception groups, respectively. For IVF/ICSI children compared with spontaneous conceptions, a significantly increased risk of CHD was observed (OR=1.45; 95% CI 1.20-1.76; p=0.0001; I2 =44%; p=0.08)
In the secondary analysis based on few available data on specific types of CHD (Figure 3), the slightly increased risk of all cardiac malformations after IVF/ICSI was not significant and seemed to be related to minor CHD than major CHD.
Minor CHD like VSD and ASD, as well as HLHS were more frequent in IVF/ICSI pregnancies than in controls, whereas TOF, TGA, and CoA were less frequent in the IVF/ICSI group as compared to the spontaneous group.

DIFFERENT TYPES OF MYOCARDIAL INFARCTIONS (MI)

According to the “Universal Definition of MI” position paper, all of these clinical settings defining acute MI may be classified into 5 types, based on pathologic, clinical, and prognostic differences.
This allocation to different types of MI grounded on their distinct pathophysiology might also justify different and individual treatment strategies.

1. MI type 1 is defined as the presence of atherothrombotic coronary artery disease resulting in an acute occlusion or relevant stenosis of a coronary vessel precipitated by atherosclerotic plaque disruption (rupture or erosion). Confirmation of the diagnosis
is based on identification of a coronary thrombus by angiography including intracoronary imaging or post mortem by autopsy.

2. Type 2 MI is also defined by the confirmation of acute myocardial ischemia, which in contrast to type 1 MI is not caused by an acute coronary plaque disruption but rather by an imbalance of myocardial oxygen supply and demand. Patients with type 2 MI might also suffer from known or presumed coronary artery disease and might thus be prone to ischemia in cases of additional acute
stress such as hemorrhagic conditions with a relevant drop of hemoglobin or sustained heart rhythm disorders. Although coronary atherosclerosis is a common finding in type 2 MI, it has to be emphasized that the presence of coronary artery disease is not a mandatory precondition for every type 2 MI. Other potential causes comprise various pathologies including severe hypoxemia, shock, coronary artery dissection, or spasm and microvascular dysfunction, for instance. Interestingly, type 2 MI has worse short and long term
outcomes as compared with type 1 MI. A large meta-analysis found a significantly higher intra hospital (15% vs 4.7%), 30 days (17.6% vs 5.3%) and 1-year mortality (27% vs 13%) and a higher rate of major adverse cardiovascular events.

HISTORY OF BIOMARKERS FOR DIAGNOSIS OF ACUTE MYOCARDIAL INFARCTION

Only 60 years ago, biomarkers were established as a tool for the diagnosis of acute myocardial infarction (MI) for the first time in
19563. At that time, measurement of serum levels of aspartate transaminase was widely used, and the proof of elevated levels entered the first World Health Organization (WHO) definition of
MI. In the 1970s, lactate dehydrogenase (LDH), creatine kinase (CK), and myoglobin were introduced and further enhanced the available spectrum of blood markers in the context of the early differential diagnosis of MI. Yet, a relevant lack of specificity of these markers limited their use. Later advances in electrophoresis allowed detection of cardiac-specific isoenzymes of CK and LDH (ie, CK-MB and LDH-1 and -2), which led to a modification of WHO criteria to rule out acute MI in 1979. Although the high rate of false positive results due to equally high positivity in the setting of skeletal muscular injury relevantly impaired their diagnostic accuracy, CK and LDH played a crucial role in the diagnosis of MI up to the 1990s.

Troponin—a protein component of myofibrils—had already been discovered in 1965. In 1989, a reliable immunoassay to detect
serum levels of cardiac troponin (cTN) levels as cardiospecific protein was developed.8 In contrast to the contemporary approach, cTN measurements were initially only used in cases of STsegment elevation MI (STEMI) to monitor infarct size. In the context of acute MI, elevated cTN levels can be detected after 4 to 10 hours after
onset of symptoms with a peak at 12 up to 48 hours and return to normal concentrations after 4 to 10 days. Test sensitivity of cTN measurements for MI was found to be as high as nearly 100% after 6 to 12 hours after symptom onset with these early assays. Thus, guidelines of the early 2000s established a rule-out strategy for patients with ACS presenting without ST-segment elevation (NSTE-ACS) based on the sequential measurements of cTN levels, repeated after 6 to 12 hours.
The cardiac troponin complex is formed by 3 subunits: troponin C, T, and I. While troponin C harbors the calcium-binding site, troponin T attaches to the actin filament and troponin I works
as inhibitor of interaction with myosin heads in the absence of calcium. Of these 3 subunits, cTNI and cTNT isoforms are specific to cardiac myocytes, and thus, their level in serum can be used as surrogate for myocardial damage.

CARCINOID HEART DISEASE

Carcinoid tumors are a rare subset of neuroendocrine tumors that originate from the gastrointestinal tract (55%) and bronchopulmonary system (30%). The incidence is 38.4 per 1 million individuals.

Carcinoid tumors have profound cardiovascular and non-cardiovascular effects caused by the release of various vasoactive substances, including serotonin, 5-hydroxytryptopan, histamine, bradykinin, tachykinins, and prostaglandins. The constellation of symptoms attributed to these effects is called the
carcinoid syndrome, which consists of flushing, hypermotility of the gastrointestinal tract, hypotension, and bronchospasm.

Carcinoid heart disease is the collective term for all cardiac manifestations that develop in patients with carcinoid malignancies, including valvular disease, heart failure, and metastatic tumor involvement.

Cardiac involvement eventually occurs in 50% of patients with carcinoid syndrome and is the presenting symptom of carcinoid disease 20% of the time. Most patients with carcinoid heart disease
present in the fifth to seventh decades of life. The right side of the heart is the most often affected, specifically the tricuspid and pulmonary valves. Progressive valvular disease leads to the development of edema, ascites, and right-sided heart failure. Carcinoid heart disease is a major cause of morbidity and mortality in patients with carcinoid syndrome. Untreated, the 3-year survival of carcinoid heart disease is 31%, approximately half the survival rate of carcinoid patients without cardiac involvement. Diagnosis and management of carcinoid heart disease are challenging, because the initial presentation can be subtle, and the disease can progress quickly leading to high morbidity.

PATHOPHYSIOLOGY OF CARCINOID HEART DISEASE

The cardiac manifestations of carcinoid tumors are attributed to the paraneoplastic effects of vasoactive substances released by the malignant cells, including 5-hydroxytryptamine (serotonin), histamine, tachykinins, transforming growth factor b (TGF-b), and prostaglandins. Normally these substances are metabolized and inactivated by the liver and lung; however, metastatic disease
involving the liver exposes the right-sided cardiac structures to large quantities of hormones. The exact mechanism of valvular disease in carcinoid syndrome is unknown. Some of these substances, including serotonin and TGF-b, are thought to
induce proliferation of fibroblasts, leading to the deposition of plaques on endocardial surfaces, including valve leaflets, subvalvular apparatus, and cardiac chambers. These plaques are made of smooth muscle cells, myofibroblasts, extracellular matrix, and an overlying endothelial layer. Plaque formation causes annular constriction, thickening of valve leaflets, and fusion of the subvalvular apparatus, eventually leading to noncoaptation of the valve leaflets and valvular regurgitation. Patients with carcinoid heart disease have significantly higher levels of serotonin, platelet serotonin, and urinary 5-hydroxyindoleacetic acid (5-HIAA) levels than carcinoid patients without cardiac involvement. Additionally, serotonergic drugs and other structurally similar medications
that activate serotonin receptors have been associated with similar valve lesions as those seen in carcinoid heart disease, supporting the involvement of serotonin in the pathogenesis of carcinoid-related valvular disease.

CARDIAC AMYLOIDOSIS - CARDIAC MRI

Due to its high-quality images, tissue characterization capabilities and non-irradiating nature, CMR is currently considered the imaging tool of choice for diagnosing and characterizing CA (Cardiac Amyloidosis).

Apart from the classical appearance of concentric LVH, there are other recognized CA, such as asymmetrical thickening or non-thickened LV walls. LV mass has been reported to be markedly increased in ATTR amyloidosis compared to the AL type. 36 The RV wall may be thickened, and the ejection fraction of both ventricles may be normal or decreased. The LA walls and interatrial septum may also be thickened, and in this regard non-contrast CMR can easily differentiate between a lipomatous hypertrophy and an infiltrative thickening of the interatrial septum.

Late gadolinium enhancement (LGE) is the cornerstone and the gold standard imaging technique for CA patients. The typical LGE pattern in CA is represented by diffuse myocardial hyperenhancement, with a dark blood pool. Some patients display circumferential hyperenhancement only in the subendocardium while in others it is transmural. Fontana et al. hypothesized that the patterns of LGE constitute steps in a continuous evolution of amyloid deposition, with progression from no LGE, to subendocardial LGE as an intermediate phase, and finally to transmural LGE.
Patients with no LGE have the most favourable
prognosis (92% chance of survival at 24 months), while patients with transmural LGE carry the worst prognosis (61% chance of survival at 24 months). 39 Within the transmural pattern, the median survival is longer for ATTR than for AL, suggesting that amyloid deposition is not the only mechanism of the disease, but the superimposed toxicity of the light chains in AL amyloidosis may also play a
role in defining the prognosis of CA patients.

Native T1 mapping
T1 mapping represents a pixelwise illustration of myocardial T1 relaxation times—an intrinsic property of each tissue. Native myocardial T1 enables diagnosis of CA to be made without the need for GBCA administration, because very high T1 values are characteristic for CA. As such, T1 mapping is an essential technique in patients with kidney failure who cannot receive contrast.

T2 mapping
T2 imaging is a well-established non-contrast technique that quantifies the myocardial oedema in a pixelwise manner and illustrates it on a map. Recently, oedema was demonstrated using T2 mapping in both types of amyloidosis but to a larger extent in AL CA. In the
same study, T2 predicted mortality in AL amyloidosis and remained significantly predictive after adjusting for ECV and NTproBNP. Interestingly, there was no relationship between T2 and prognosis in ATTR amyloidosis, suggesting that oedema is a less important factor in the pathogeny of ATTR than AL amyloidosis.

CARDIAC AMYLOIDOSIS - Echocardiography Features

Amyloidosis is a systemic infiltrative disease, in which proteins with unstable structure misfold, form aggregates and amyloid fibrils which can deposit in various organs: heart, kidneys, liver, gastrointestinal tract, nervous system structures, lungs, or soft tissue.

Cardiac Amyloidosis is generally classified as a restrictive cardiomyopathy (RCM) due to its pathophysiology, which frequently presents in a stage of left ventricular (LV) or biventricular hypertrophy with a small LV cavity and, sometimes in the late stages, dilatation. This is why it is also regarded as one of the hypertrophic cardiomyopathies (HCMs) phenocopies

# ECHOCARDIOGRAPHY

*** The typical echocardiographic findings in CA include a small left ventricle with concentric hypertrophy, which can have a ‘sparkling’ or ‘granular’ myocardial appearance, with a preserved ejection fraction and biatrial enlargement.

Often diagnosed when LV wall thickness is above 13 mm, it has been proven that values above 15 mm carry prognostic significance.
An important observation is the low electrocardiographic voltage-to-mass ratio.
Left ventricular ejection fraction (LVEF) is usually normal (>50%), however, it can progressively decrease in late stages of the disease.
** Even at early stages subclinical systolic dysfunction can be detected using tissue Doppler imaging (TDI)—as myocardial systolic (S' ) and diastolic (e' ) longitudinal velocities are low in CA. Subclinical systolic dysfunction, which precedes the onset of heart failure symptoms, can be detected by strain and strain rate imaging, even before TDI parameters are altered.
Using speckle tracking echocardiography, regional
variations in 2D longitudinal strain (LS) from base to apex is seen, and defined as ‘relative apical sparing’ calculated as the ratio of apical LS to the sum of basal and mid LS

All the 2D speckle-tracking derived LA phasic functions were severely impaired in CA and highly correlated with LV deformation, being correlated with a greater impairment of LV systolic and diastolic function.
Absent atrial contractility can lead to intra-atrial thrombus formation even in sinus rhythm patients. Awareness of this complication is crucial for timely initiation of anticoagulant therapy. A large autopsy study of patients with CA 31 reported a high incidence of intracardiac thrombosis (most frequently atrial), especially in AL patients, despite sinus rhythm and relatively preserved LVEF. The AL type, co-existence of AF, poor LV diastolic function, RV wall thick-
ness, and higher heart rates were all independent predictors for systemic thromboembolism.

VASOSPASTIC ANGINA / MICROVACSCULAR ANGINA

**It is Important to note, that obstructive coronary artery disease, coronary spasm, and coronary microvascular dysfunction can coexist in the same patients; this is why in a sizable proportion of patients angina persists after successful coronary revascularization.

Among patients with documented vasospastic angina in the absence of obstructive coronary artery disease, about half complains of effort-related angina. 5 Among patients with
microvascular angina chest pain can occur at rest and on exercise because the two pathogenetic mechanisms of ischaemia, microvascular spasm, and impaired microvascular dilatation frequently coexist.

*** Diagnostic criteria for vasospastic angina
(i) nitrate-responsive rest angina;
(ii) transient ischaemic electrocardiogram (ECG) changes during spontaneous angina;
(iii) in the absence of documentation of ischaemia during rest angina, documentation of coronary artery spasm, defined as transient total or sub-total coronary artery occlusion (>90% constriction) with angina and ischaemic ECG changes either spontaneously or in response to a
provocative stimulus (typically acetylcholine).

*** Diagnostic criteria for microvascular angina
(i) presence of symptoms suggestive of myocardial ischaemia;
(ii) objective documentation of myocardial ischaemia during stress, as assessed by currently available techniques;
(iii) absence of obstructive coronary artery disease
(_0.80); and
(iv) documentation of a reduced coronary blood flow reserve and/or inducible microvascular spasm.
In turn, the documentation of microvascular spasm during provocative testing with acetylcholine is based on stringent criteria: (i) lack of epicardial coronary spasm; (ii) reproduction of anginal symptoms experienced by the patient during his daily life; and (iii) transient ischaemic changes on 12-lead ECG.

Thus, in a patient with suspected angina, a diagnostic workup which comprehensively assesses both anatomic and functional alterations of coronary circulation is needed to convincingly exclude or confirm the diagnosis of angina

LIPID PROFILE AND HEART DISEASE

Plasma LDL-C is a measure of the cholesterol mass carried by LDL particles, by far the most numerous of the ApoB-containing lipoproteins, and is an estimate of the concentration of circulating LDL
LDL-C is causally associated with the risk of Atherosclerotic Heart Disease, and that lowering LDL-C reduces the risk proportionally to the absolute achieved reduction in LDL-C

** The clinical benefit of lowering LDL-C is determined by the reduction in circulating LDL particles as estimated by ApoB, which is usually mirrored by a reduction of cholesterol carried by those particles. Therefore, the clinical benefit of therapies that lower LDL-C by reducing LDL particle mass will be proportional to the absolute reduction in LDL-C, because on average the reduction in LDL-C and LDL particles will be concordant.

the plasma TG concentration reflects the concentration of circulating ApoB-containing TG-rich lipoproteins. Elevated plasma TG levels are associated with an increasing risk of
Atherosclerotic heart disease.

LIPID PROFILE
Total Cholesterol in humans is distributed primarily among
three major lipoprotein classes: VLDL, LDL, and HDL. Smaller amounts of cholesterol are also contained in two minor lipoprotein classes: IDL and Lp(a). A standard serum lipid profile measures the concentration of TC and HDL-C, as well as TG. With these values, the LDL-C concentration can be estimated.

Fasting or non-fasting?
Traditionally, blood sampling for lipid analyses has been recommended in the fasting state. Recent systematic studies comparing fasting and non-fasting samples have suggested that the difference is small for most lipid parameters. Non-fasting sampling has been used in large population-based studies. 100 In most studies, non-fasting samples display a higher TG level of 0.3 mmol/L (27mg/dL). On average, and for most individuals, this increment will be
of no clinical significance. Indeed, a number of guidelines recommend non-fasting sampling.

LIPIDS & ATHEROSCLEROSIS
Role of lipids in the
pathophysiology of atherosclerosis

All ApoB-containing lipoproteins