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Left ventricular noncompaction

Dalam dokumen A Comprehensive Guide for Clinicians (Halaman 184-188)

Left ventricular noncompaction refers to the presence of a thickened two-layer myocardium with a compacted epicardial layer and a noncompacted trabeculated endocardial layer of at least twice the thickness. It is unclear whether this represents a distinct cardiomyo- pathy or is simply a feature of many.[ 1 ] Th e prevalence is unknown but it is increasingly being diagnosed on echocardiogram or cardiac MRI. Clinical presentation varies: aff ected individuals may be asymptomatic or pre- sent with heart failure, thromboembolism, or arrhyth- mia. Th ere is case report evidence on pregnancy in left ventricular non-compaction,[ 2 ] with outcomes vary- ing from good to severe heart failure, as expected from the range of clinical severity in the nonpregnant state.

Management in pregnancy should therefore, in the absence of current disease specifi c knowledge, be based on left ventricular function, arrhythmia risk, and thromboembolic risk. Th ere is currently no evidence to support routine full anticoagulation .

References

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Section 4: Antenatal Care: Specifi c Maternal Conditions

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Heart Disease and Pregnancy, 2nd edn. ed. Philip J. Steer and Michael A. Gatzoulis. Published by Cambridge University Press.

© Cambridge University Press 2016.

Chapter

Antenatal Care: Specifi c Maternal Conditions

Section 4

Practical practice points

1. An acute myocardial infarction during

pregnancy can be missed because it is mistaken for a variety of more common causes of chest pain, such as acid refl ux and musculoskeletal disorders. Th e diagnosis should therefore be considered, and investigated appropriately, in any woman presenting with chest pain in pregnancy.

2. Prompt diagnosis and treatment with

percutaneous coronary intervention are necessary to reduce the currently high maternal and perinatal mortality.

3. Coronary dissection seems to be a more frequent cause of myocardial infarction during pregnancy than atherosclerosis or thrombus formation.

4. Th rombolytic therapy can be given but serious adverse eff ects, especially bleeding complications, have been reported.

5. Radiation exposure of the fetus during angiography and percutaneous coronary intervention appears to be low; if possible, it is preferably postponed to beyond the 15th week of pregnancy.

6. All pregnant women with angina or myocardial infarction should be treated by a multidisciplinary team in a tertiary center .

Introduction

Th e prevalence of coronary artery disease in women is increasing owing to changing patterns of lifestyle, including cigarette smoking, diabetes, overweight, and stress. In 1989, it was reported that approximately 10%

of women with myocardial infarction were under the age of 40 years.[ 1 ] Since then, women have increasingly

been having their fi rst pregnancy at a later age, and a higher incidence of acute myocardial infarction dur- ing pregnancy is therefore to be expected in the future.

When infarction occurs in pregnancy, it constitutes a particular problem because the selection of diagnos- tic and therapeutic approaches is greatly infl uenced not only by maternal but also by fetal considerations.

Th e risk of a myocardial infarction in women during pregnancy was estimated in 2006 as 6.2 per 100 000 deliveries, which is 3–4 times higher than in young women outside pregnancy.[ 2 ] Myocardial infarction can occur at all stages of pregnancy, but there is a clear peak of incidence in the third trimester. Th e majority of pregnant women suff ering from myocardial infarc- tion are older than 30  years.[ 3 , 4 ] Other risk factors for pregnancy-associated myocardial infarction are thrombophilia, hypertension, smoking, transfusion, diabetes, and postpartum infection. [ 2 ]

In normal pregnancy, circulatory changes not only ensure the adequate supply of nutrients and oxygen to the developing fetus but also change the load on the cardiac muscle. Blood volume and cardiac output increase by 40–45%. Th is increase peaks at around the 24–26th weeks of gestation and stays high or slowly decreases thereaft er until term. Furthermore, there is an increase in heart rate of 20–25 beats/min through- out the entire pregnancy. Gestational hormones and circulating prostaglandins, in combination with the low vascular resistance of the placenta and the uterus, decrease both the peripheral vascular resistance and blood pressure. During labor, the uterine contrac- tions result in a further increase in cardiac output.

Finally, aft er delivery, there is a signifi cant increase in cardiac preload as a result of decompression of the inferior vena cava and the return of uterine and placental blood into the circulation. Reabsorption of

Management of ischemic heart disease

Dalam dokumen A Comprehensive Guide for Clinicians (Halaman 184-188)