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Diagnostic evaluation of acute pancreatitis in two patients with hypertriglyceridemia.

We present two diagnostically challenging cases of acute pancreatitis with hypertriglyceridemia accompanied with chylomicronemia caused with a deficiency of lipoprotein lipase and with the presence of type V hyperlipidemia. Both cases suffered from acute abdomen following the ingestion of fatty food and revealed the increase in parameters of inflammation without significant elevation of serum amylase levels. The imaging examination of ultrasonography could not detect significant findings of acute pancreatitis and a computer tomography scan eventually confirmed the findings of acute pancreatitis. Both cases responded to a low fat diet and administration of a cholecystokinin receptor antagonist, exhibiting a relief of abdominal symptoms. As in the present cases with acute abdomen following the ingestion of fatty food, the identification of serum hypertriglyceridemia and an abdominal computer tomography scan might be useful in establishing the diagnosis of acute pancreatitis and in developing the therapeutic regimen, when hypertriglyceridemia interferes with the evaluation of pancreatic enzyme activities and ultrasound examination provides poor pancreatic visualization.

Acute Disease↗

[A study of hypertriglyceridemia occurring in patients with chronic hepatitis C during administration of interferon beta].

The prevalence and risk factors of hypertriglyceridemia during the administration of interferon (IFN) were examined in 78 patients with chronic hepatitis C who were treated with 6 MU of IFN-beta once or 3 MU of IFN-beta twice a day for 6 weeks. Hypertriglyceridemia (serum triglyceride (TG) above 150 mg/dl) was found before the start of IFN treatment in 9% of the patients. During the administration of IFN, elevation of serum TG above 150 mg/dl was found in 82% of patients. In addition, serum TG level exceeded 500 mg/dl at least once during the administration of IFN in 13% of patients. On stepwise multiple regression analysis, three risk factors, high serum TG value before the administration of IFN, high ALT value before the administration of IFN, and divided administration of IFN-beta twice daily were found to be associated with hypertriglyceridemia during IFN administration.

Adult↗

Two novel mutations in the lipoprotein lipase gene in a family with marked hypertriglyceridemia in heterozygous carriers. Potential interaction with the polymorphic marker D1S104 on chromosome 1q21-q23.

Two novel mutations in the lipoprotein lipase (LPL) gene are described in an Austrian family: a splice site mutation in intron 1 (3 bp deletion of nucleotides -2 to -4) which results in skipping of exon 2, and a missense mutation in exon 5 which causes an asparagine for histidine substitution in codon 183 and complete loss of enzyme activity. A 5-year-old boy who exhibited all the clinical features of primary hyperchylomicronemia was a compound heterozygote for these two mutations. Nine other family members were investigated: seven were heterozygotes for the splice site mutation, one was a heterozygote for the missense mutation, and one had two wild-type alleles of the LPL gene. LPL activity in the post-heparin plasma of the heterozygotes was reduced to 49;-79% of the mean observed in normal individuals. Two of the heterozygotes had extremely high plasma triglyceride levels; in three of the other heterozygotes the plasma triglycerides were also elevated. As plasma triglycerides in carriers of one defective LPL allele can be normal or elevated, the heterozygotes of this family have been studied for a possible additional cause of the expression of hypertriglyceridemia in these subjects. Body mass index, insulin resistance, mutations in other candidate genes (Asn291Ser and Asp9Asn in the LPL gene, apoE isoforms, polymorphisms in the apoA-II gene and in the apoAI-CIII-AIV gene cluster, and in the IRS-1 gene) could be ruled out as possible factors contributing to the expression of hypertriglyceridemia in this family. A linkage analysis using the allelic marker D1S104 on chromosome 1q21;-q23 suggested that a gene in this region could play a role in the expression of hypertriglyceridemia in the heterozygous carriers of this family, but the evidence was not sufficiently strong to prove this assumption. Nevertheless, this polymorphic marker seems to be a good candidate for further studies.

Adult↗

[Acipimox (Olbetam) as a secondary hypolipemic agent in combined hypertriglyceridemia and hyperlipidemia].

32 patients with hypertriglyceridemia, excessive hypertriglyceridemia, and combined hyperlipidemia, were treated with the nicotinic acid derivative acipimox (Olbetam). First line treatment with bezafibrate, or statins in some with combined hyperlipidemia, had failed. In 10 acipimox was discontinued due to side effects or absence of clinical response. The other 22 completed 6 months of treatment with no side effects. Acipimox caused a significant 54% decrease in triglyceride levels, a 23% decrease in total cholesterol, and a 12% increase in HDL-cholesterol. LDL-cholesterol was difficult to calculate because of the high triglyceride levels, so no results are presented. Although acipimox was much better tolerated than nicotinic acid, it also had side effects, but fewer. Acipimox can therefore be used as a second-line drug, mainly in those with combined hyperlipidemia and hypertriglyceridemia.

Adult↗

Neonatal chemical sympathectomy attenuates fructose-induced hypertriglyceridemia and hypertension in rats.

Experiments were performed to determine the pathogenic contribution of the peripheral sympathetic nervous system to fructose-induced hypertriglyceridemia, hyperinsulinemia and hypertension in rats. Neonatal chemical sympathectomy was performed in neonatal Sprague-Dawley rats (1-week old) by administration of guanethidine (50 microg/g, i.p.) 5 times per week for consecutive 3 weeks and nerve-intact rats were served as controls. Both groups of rats were fed a fructose-enriched diet for 9 weeks. The systolic blood pressure (SBP) and body weight were measured weekly and arterial blood samples were taken weekly for determinations of plasma insulin, glucose and triglyceride levels. The results showed that fructose feeding for one week significantly increased SBP in intact rats and sympathectomized rats (116+/-1 to 119+/-1 mmHg and 116+/-1 to 120+/-1 mmHg, respectively). SBP further increased thereafter in both groups. However, the increased SBP levels were significantly higher in intact group than in sympathectomized group after 5 weeks of fructose feeding. Fructose feeding for one week concurrently produced hypertriglyceridemia that preceded the appearance of hyperinsulinemia in both groups. The elevated plasma triglyceride levels were significantly lower in sympathectomized rats than in intact rats after 3 weeks of fructose feeding, whereas the elevated plasma insulin concentrations were not different between groups throughout fructose feeding period. Plasma glucose concentrations of both groups were comparable and remained unchanged throughout the study. These data indicate that neonatal chemical sympathectomy attenuated, but did not prevent, fructose-induced elevations in blood pressure and plasma triglyceride levels, suggesting a partial dependency of fructose-induced hypertriglyceridemia and hypertension on the integrity of the peripheral sympathetic nervous system (SNS) in rats.

Animals↗

Hypertriglyceridemia: a review of clinical relevance and treatment options: focus on cerivastatin.

The triglyceride (TG) level is one of several lipid parameters that can aid prediction of coronary heart disease (CHD) risk. An elevated plasma TG level is strongly associated with an increased risk of CHD. Hypertriglyceridemia, the second most common dyslipidemic abnormality in hypertensive subjects after increased low-density lipoprotein cholesterol (LDL-C), is defined by the National Cholesterol Education Programme (NCEP) as a fasting TG level of > 2.26 mmol/l (> 200 mg/dl) and is recognised as a primary indicator for treatment in type IIb dyslipidemia. Raised TG levels can be present in individuals at risk for CHD when the total cholesterol is normal. However, not all individuals with raised TG levels have increased risk of CHD. Factors such as: diet, age, lifestyle, and a range of medical conditions, drug therapy and metabolic disorders, can all affect the TG level. In some of these circumstances, other factors protect against the risk of CHD, and can minimise or negate the effect of the risk factors present. Although TG reducing therapy has been shown to be associated with an improved clinical outcome, more research is needed to determine whether this is an independent effect of TG reduction or an effect of normalising the overall lipid profile in hypertriglyceridemic patients. Further trials are required to quantify the clinical benefits of lowering TG to 'target' levels and to confirm targets defined by NCEP-II (shown in Table 1). The role of TG in CHD pathogenesis is thought to involve several direct and indirect mechanisms, such as effects on the metabolism of other lipoproteins, transport proteins, enzymes, and on coagulation and endothelial dysfunction. More research is required to fully elucidate the role of TG, the ways in which it can influence other risk factors and the mechanism of its own more direct role in the atherogenic process. Patients with hypertriglyceridemia have been shown to respond well to dietary control and to the use of lipid lowering drugs such as 3-hydroxy-3-methylglutaryl-Coenzyme A (HMG CoA) reductase inhibitors (known as statins), fibrates and nicotinic acids. However, recent retrospective real-life clinical studies show that only 38% of patients receiving some form of lipid-lowering therapy achieved NCEP-defined LDL-C target levels, demonstrating the need for the use of more aggressive treatment. In hypertriglyceridemic patients, the newer statins, cerivastatin and atorvastatin, have shown comparable efficacy in reducing TG compared with the older statins. Achieving NCEP target lipid levels has been shown to reduce the risk of cardiovascular disease in dyslipidemic individuals, including high-risk patient groups such as those with additional risk factors, existing heart disease, diabetes mellitus and metabolic syndrome. Although the latest clinical studies investigating combination therapies, i.e. dual therapy with both a statin and a fibrate, have demonstrated them to be effective for overall control of lipid parameters and reducing coronary events, it is not yet clear whether this offers any significant advantage over monotherapy. Results from ongoing longer-term end-point clinical studies may provide further information in this area and consequent reviews of primary care management policies for dyslipidemia. Statin monotherapy may be a reliable option for primary care treatment of dyslipidemia (including hypertriglyceridemia).

Atorvastatin↗

[heparin and insulin treatment of acute pancreatitis caused by hypertriglyceridemia. Experience of 5 cases].

BACKGROUND: Hypertriglyceridemia over 1,000 mg/dl can provoke acute pancreatitis and its persistence can worsen the clinical outcome. On the contrary, a rapid decrease in triglyceride level is beneficial. Plasmapheresis has been performed in some patients to remove chylomicrons from the circulation, while heparin and/or insulin have been administered in some other cases to rapidly reduce blood triglycerides. Heparin and insulin stimulate lipoprotein-lipase activity and accelerate chylomicron degradation. AIM: To report five patients with acute pancreatitis treated with heparin and insulin. PATIENTS AND METHODS: Five patients (4 females and 1 male) seen in the last two years, who suffered acute pancreatitis induced by hypertriglyceridemia are reported. Initial blood triglyceride levels were above 1,000 mg/dl (range 1,590-8,690 mg/dl). Besides the usual treatment of acute pancreatitis, heparin and/or insulin were administered intravenously in continuous infusion. Heparin dose was guided by usual parameters of blood coagulation, and insulin dose, by serial determinations of blood glucose. Pancreatic necrosis was demonstrated in 4 patients. RESULTS: Serum triglyceride levels decreased to < 500 mg/dl within 3 days in all cases. No complication of treatment was observed and all patients survived. Early and late complications of pancreatitis occurred in one patient. CONCLUSION: Administration of heparin and/or insulin is an efficient alternative to reduce triglyceride levels in patients with acute pancreatitis and hypertriglyceridemia.

Acute Disease↗

Postprandial hypertriglyceridemia in non-diabetic patients with coronary artery disease.

BACKGROUND: Hypercholesterolemia has been established as a major independent risk factor for coronary artery disease, but the role of hypertriglyceridemia, is still controversial in this regard. Postprandial hypertriglyceridemia has been reported to be a predisposing factor for coronary events. Present study was undertaken to assess postprandial hypertriglyceridemia in non-diabetic patients with coronary artery disease. METHODS AND RESULTS: 60 subjects aged over 35 years, who had undergone coronary angiography, were included in this case-control study. Subjects having secondary hyperlipidemia were excluded. The case group had significant stenosis in at least one coronary artery while the control group had normal coronary arteries on angiography. Triglyceride level was evaluated in fasting non-stressful situation as well as three hours after a heavy breakfast (bread, butter and jam, approximately 460 kcal). It was defined as normal (<150 mg/dl), borderline (150-200 mg/dl) and high (>200 mg/dl) according to NCEP guidelines, 2001. The mean fasting triglyceride level in control and case group was 141+/-54 v. 162+/-60 mg/dl respectively (statistically not significant). The mean postprandial triglyceride level, in control and case group was 163+/-60 v. 265+/-98 mg/dl, respectively (p<0.05). In the case group, 63.3%, 3.3%, and 33.3%, and in the control group 70%, 16.7% and 13.3% had normal, borderline and high fasting triglyceride levels, respectively (p<0.05). 3.3%, 23.3%, 73.3% of the cases and 50%, 36.7%, 13.3% of the controls had normal, borderline and high postprandial triglyceride levels, respectively (p<0.05). CONCLUSIONS: Considering that the triglyceride levels were higher in postprandial state, fat tolerance test can be used as a complementary test in evaluation of lipid profile in patients with coronary artery disease with normal fasting triglyceride levels.

Adult↗

Associations between hypertriglyceridemia and serum ghrelin, adiponectin, and IL-18 levels in HIV-infected patients.

HIV-related metabolic abnormalities include hypertriglyceridemia, hypercholesterolemia, insulin resistance, and diabetes mellitus. Recent studies suggest a role of ghrelin in promoting the deposition of triglycerides (TG) in the liver and regulating the metabolic action of adiponectin. Visceral fat is a key regulator of inflammation and it secretes proinflammatory cytokines (eg, interleukin-18, IL-18), with potential atherogenic activity. The aim of this study was to assay serum concentrations of ghrelin, adiponectin, and IL-18 in HIV+ patients, with and without hypertriglyceridemia, who were receiving highly active antiretroviral therapy (HAART). The 49 HIV+ patients were divided in 2 groups: 17 patients with serum TG concentration >200 mg/dl (group A) and 32 patients with normal serum TG concentration (group B). All subjects underwent viral and immunological evaluations and determinations of serum cholesterol, glucose, ghrelin, adiponectin, and IL-18. No differences of viral and immunological parameters were observed between the 2 groups. Serum levels of ghrelin were 768 +/- 596 pg/dl in group A and 470 +/- 248 pg/dl in group B (p = 0.01). Group A had lower serum adiponectin levels (8.4 +/- 3.6 microg/dl) than group B (18.2 +/- 10.1 microg/dl; p = 0.0001). Serum IL-18 levels were 455 +/- 199 pg/ml in group A and 258 +/- 233 pg/ml in group B (p = 0.005). The patients with hypertriglyceridemia showed a positive correlation between serum triglyceride and ghrelin levels (r = 0.51, p = 0.03). These findings suggest potential roles of ghrelin, adiponectin, and IL-18 in the pathogenesis of metabolic disorders in HIV-infected patients.

Adiponectin↗

Capecitabine-induced hypertriglyceridemia: a report of two cases.

BACKGROUND: Capecitabine is a tumor-activated oral fluoropyrimidine with established antitumor activity in breast and colorectal cancer. Hypertriglyceridemia associated with this drug has rarely been reported in the literature. CASE REPORT: This is a report of two patients who developed capecitabine-induced severe hypertriglyceridemia, together with an increase in total cholesterol levels. The first patient developed hyperlipidemia during long-term capecitabine treatment in combination with trastuzumab for metastatic breast carcinoma (triglycerides: from 219 mgldl to 1409 mg/dl, 543% increase; cholesterol: from 239 mg/dl to 363 mg/dl, 52% increase). The second patient developed abnormalities in the lipid profile after the second cycle of chemotherapy with capecitabine and oxaliplatin for metastatic colorectal cancer (triglycerides: from 101 mg/dl to 1510 mg/dl, 1395% increase; cholesterol: from 203 mg/dl to 310 mgldl, 52% increase). An analysis of the possible underlying pathogeneic mechanisms is provided. CONCLUSION: Physicians should be aware of the possibility of dyslipidemia, particularly hypertriglyceridemia, following treatment with capecitabine.

Aged↗

Association of two genetic variations of lipoprotein lipase, S447X and Hind III, with coronary artery disease and hypertriglyceridemia.

This study was performed to assess the effect of the S447X and Hind III lipoprotein lipase gene polymorphisms on development of coronary artery disease and hypertriglyceridemia. The study included 132 patients and 98 healthy control subjects of Croatian descent. The lipoprotein lipase S447X polymorphism was associated with coronary artery disease and hypertriglyceridemia, as indicated by the lower frequency of S447 allele in the patient group (p = 0.005) and odds ratio (O.R = 0.40, p = 0.006). The patient and control groups also showed a significant difference in the distribution of Hind III/S447X genotype combinations (p = 0.013). There were no significant associations with lipid parameters for any genotype or genotype combination in the patient group. Frequencies of the S447X polymorphism and S447X/Hind III combinations differed between the CAD/TG and control group, thus these polymorphisms may be associated with CAD and hypertriglyceridemia.

Adult↗

[Pathogenesis of alcohol-induced hyperlipidemia: case report of hypertriglyceridemia over 10,000 mg%].

A 53-year old woman developed excessive hypertriglyceridemia (greater than 10,000 mg/dl) with features of toxic liver damage after prolonged ethanol ingestion. Lipoprotein-lipase-activity was not decreased, apolipoprotein-C-II analysis, as shown by gel-electrophoresis, revealed a regular pattern. Treatment with parenteral nutrition and abstinence of ethanol resulted in a complete normalization of plasma triglycerides after transient remnant-hyperlipidemia. Decrease of triglycerides was accompanied by declining liver enzyme activities. As suggested by unimpaired activity of lipolysis, the extent of hypertriglyceridemia may be explained by a reversible receptor mediated defect of hepatic catabolism, aggravated by hepatic overproduction of triglyceride-rich-particles. Although receptor dysfunction is not yet understood, the transient appearance of remnant particles may be a helpful criteria in diagnosis of ethanol induced hypertriglyceridemia.

Alcoholism↗

[Efficacy and tolerability of simvastatin and omega-3 fatty acid combination in patients with coronary disease, hypercholesterolemia and hypertriglyceridemia].

Patients with ischemic heart disease are often affected by a mixed hyperlipoproteinemia, where a hypercholesterolemia of various severity is accompanied by slight or moderate hypertriglyceridemia (type IIb dyslipidemia). Current epidemiologic evidence suggests that hypertriglyceridemia has not to be disregarded, particularly in certain subgroups of patients. We evaluated the effect of the association of simvastatin 10 mg/day [an hydroxymethyl-glutaryl-CoA (HMG-CoA) reductase inhibitor] and omega-3 polyunsaturated fatty acids (n3-PUFA) in comparison with simvastatin 10 mg/day alone. The subjects undergoing the study were affected by coronary artery disease and showed hypercholesterolemia (LDL-cholesterol > 160 mg/dl) and moderate hypertriglyceridemia (serum triglycerides 200-400 mg/dl) after 2 months of moderate dietary therapy for hyperlipidemia (Step 1 of the National Cholesterol Education Program [NCEP]). Thirty-nine patients were randomized to have 1 of 2 scheduled treatments. At the same time the patients underwent severe dietary therapy for hyperlipidemia (Step 2 of the NCEP). After 3 months of treatment, total-cholesterol, LDL-cholesterol, and triglycerides were significantly lower than basal values in both groups (p < 0.05). Total-cholesterol, LDL-cholesterol, and triglycerides were lower in the group treated with n3-PUFA and simvastatin compared to simvastatin alone. However, only for triglycerides was the difference significant (-39.99% in patients treated with n3-PUFA and simvastatin versus -25.65% in patients treated with simvastatin alone, particularly in the first group of 35.85%; p < 0.05). With regard to HDL-cholesterol, the differences between the basal values and the 2 groups of treatments were non significant. Remarkable side effects were not observed in the 2 groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

[Acute pancreatitis in newly diagnosed type I diabetes mellitus with diabetic ketoacidosis and hypertriglyceridemia].

A 19 years old patient who presented grade D acute pancreatitis by abdominal CT with marked hypertriglyceridemia during a diabetic ketoacidosis (DKA) in the onset of a type I diabetes mellitus is described. The pancreatitis and DKA were resolved with the usual treatment, and the levels of triglycerides became normal within one week. Hyperamylasemia is frequent in DKA although of uncertain significance. Acute pancreatitis coinciding with DKA has been described, in this case radiologic findings demonstrated the diagnosis. No other bibliographic references have been found in which pathologic imaging in abdominal CT are described in a situation of DKA with hyperamylasemia. Moderate hypertriglyceridemia is common upon initiation of diabetes mellitus and likewise it usually presents during the course of acute pancreatitis. Pancreatitis could be secondary to hypertriglyceridemia and the latter to the insulin deficiency.

Acute Disease↗

A case of moderate hypertriglyceridemia with apolipoprotein E phenotype E4/3.

Hyperlipoproteinemic subjects with apo(lipoprotein)E4 are usually hypercholesterolemic and those with apoE2 are hypertriglyceridemic. We report a case of moderate hypertriglyceridemia with apoE phenotype E4/3. Plasma levels of total cholesterol (TC), triglyceride (TG), high density lipoprotein (HDL)-C, apoAI, apoB, apoCII, apoCIII, and apoE were 200mg/dL, 451 mg/dL, 31 mg/dL, 115 mg/dL, 99 mg/dL, 10.0 mg/dL, 22.2 mg/dL, and 12.0 mg/dL, respectively. Plasma levels of very low density lipoprotein (VLDL)-C and intermediate density lipoprotein (IDL)-C were high, and those of low density lipoprotein (LDL)-C and HDL2-C were low. All lipoprotein subfractions except VLDL were TG-rich. These findings are common in moderate hypertriglyceridemia. The plasma level of remnant-like particle (RLP, equivalent to chylomicron remnant)-C, was high. The lipoprotein lipase which removes TG from chylomicron and VLDL was normal. The activity of LDL receptor which removes remnants of chylomicron and VLDL as well as LDL was high. ApoE4 actively binds to receptors of remnant and LDL. Thus, the removal of TG-rich lipoproteins should not be impaired in this patient. Plasma levels of insulin during oral glucose tolerance test were high. Hyperinsulinism stimulates VLDL synthesis in the liver. Subjects with apoE4 show active synthesis of chyromicron. Thus, we concluded that the moderate hypertriglyceridemia in this E4/3 patient was due to the overproduction of chylomicron and VLDL.

Adult↗

Juvenile familial hypertriglyceridemia and growth retardation. Clinical and biochemical observations in three siblings.

Familial hypertriglyceridemia or hyperlipoproteinemia type I was detected in three siblings aged 6, 11, and 14 of an otherwise normal Turkish family of 10 members. Initial values ranged from 1780 to 3750 mg/100 ml triglycerides in the milky white serum; cholesterol was normal. Lipoprotein pattern on agarose and acrylamide gel revealed a heavy band of chylomicrons and missing HDL; post-heparin lipolytic activity was decreased to about 30% of normal. Chylomicronemia could be induced by a fat-rich (50% of total calories) diet, but not by carbohydrates. On a low fat diet (5%) during hospitalization chylomicrons disappeared, and triglycerides decreased to about 450 mg/100 ml. Phenocopies of hypertriglyceridemia could be excluded. All three patients were the only members of the family who were small, below the third percentile. Their bone age was retarded from 18 to 30 months. There was no indication for an endocrine cause of the growth retardation: four different stimulation tests revealed normal growth hormone response, thyroid and adrenal functions were not impaired; sexual development was normal. Increased glucose assimilation was observed during intravenous and oral glucose load. Peak serum insulin response was above normal during stimulation tests. The possible etiologic role of hypertriglyceridemia in this concomitant growth retardation is discussed.

Adolescent↗

[Diurnal patterns of plasma lipids and lipoproteins in primary endogenous hypertriglyceridemia (type IV-hyperlipoproteinemia) (author's transl)].

Acute and chronic effects of three isocaloric diets on plasma lipids and plasma lipoproteins were studied in 10 patients with primary endogenous hypertriglyceridemia (type IV-hyperlipoproteinemia). The diets used contained 20% protein, 50, 37 and 1% fat and 30, 43 and 79% carbohydrates respectively. Cholesterol levels were similar with all diets. Fasting values of plasma triglycerides were lower with the fat-containing diets compared to the high-carbohydrate diet. Diurnal patterns, however, were significantly higher with the former diets in 8 of the 10 patients. Postprandial lipoprotein patterns on fat-containing diets are characterized by chylomicronemia and marked changes of concentration and composition of other lipoprotein classes. If, analogous to diabetic therapy, control of hypertriglyceridemia is meant to imply low all-day levels rather than low fasting levels, a rather low-fat, high-carbohydrate diet seems to be superior in most patients with endogenous hypertriglyceridemia to diets containing more than 35 calorie per cent of fat.

Cholesterol↗

The effects of acute hypertriglyceridemia and high levels of free fatty acids on left ventricular function.

The effects of acute hypertriglyceridemia and of high levels of free fatty acids on the left ventricular ejection fraction were studied by radionuclide ventriculography in 20 subjects with and without coronary artery disease. An infusion of approximately 125 ml of a 20% fat emulsion over 25 minutes resulted in an increase of plasma triglycerides to the mean of 820 mg/dl and a fall of the left ventricular ejection fraction from the baseline mean of 62% to 58% (p less than 0.05). Ninety minutes after the intravenous administration of 5000 units of heparin, plasma free fatty acids rose to the mean of 4.6 mmol/L and the mean left ventricular ejection fraction increased to 69% (p less than 0.001). The observed changes in blood lipids were not associated with clinical or ECG evidence of myocardial ischemia. We conclude that acute hypertriglyceridemia causes slight depression of left ventricular performance, while high levels of free fatty acids augment it. However, neither hypertriglyceridemia per se nor its rapid conversion to free fatty acids are likely to cause angina in stable patients with coronary artery disease.

Aged↗