Eclampsia and the Heart

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Saudi Med J. 2006 Oct;27(10):1526-9.
Second trimester cardiac output and its predictive value for preeclampsia.
Kazerooni T, Khosropananh S.
No. 313 Nouavaran Ave, Farzanegan Street, PO Box 71948-95897, Shiraz, Iran. Tel. +98 (711) 6262680. Fax. +98 (711) 6288427.

OBJECTIVE: To predict women at risk of preeclampsia in the second trimester by the assessment of maternal cardiac output (CO). METHODS: Between October 2001 to November 2003, we carried out a cross-sectional, prospective, hospital-base study in Shiraz University of Medical Sciences, Shiraz, Iran. Cardiac output was measured in 102 normotensive women at gestational age 19-25 weeks by Doppler echocardiography. Patients with CO >7.4 L/min were considered high risk group (Group 1) and those with CO

Eur J Heart Fail. 2005 Oct;7(6):1057-8.
Pre-eclampsia with acute heart failure postpartum as primary manifestation of systemic lupus erythematosus.
Hildbrand P, Eigenmann C, Gugger M, Marti HP, Hullin R.
Department of Cardiology, University Hospital, CH-3010 Bern, Switzerland.

Pre-eclampsia occurs in 2-5% of pregnancies of healthy women. Here, we present a rare case of pre-eclampsia with overt acute heart failure, which was the primary manifestation of systemic lupus erythematosus with cardiac and renal involvement.

Am J Hypertens. 2005 Oct;18(10):1306-12.
Comment in: Am J Hypertens. 2005 Oct;18(10):1266-70.

Peripartum hypertension from pheochromocytoma: a rare and challenging entity.
Kamari Y, Sharabi Y, Leiba A, Peleg E, Apter S, Grossman E.
Department of Internal Medicine D and Hypertension Unit, The Chaim Sheba Medical Center, Tel-Hashomer, Affiliated to the Sackler School of Medicine, Tel-Aviv University, Israel.

BACKGROUND: Pheochromocytoma, a rare and usually curable cause of hypertension, is characterized by symptoms and signs related to increased catecholamine secretion. Pregnancy can elicit clinical manifestations of otherwise unrecognized pheochromocytoma. METHODS AND RESULTS: Four women, ranging in age from 27 to 37 years, were referred to the hypertension clinic with the following presentations: 1) a 35-year-old woman, diagnosed with gestational hypertension and headaches during the third trimester of her pregnancy and 5 months after delivery, was hospitalized with pulmonary edema. Echocardiography revealed severe dilated left ventricular (LV) dysfunction. Cardiac function was normalized after surgical resection of a pheochromocytoma from her left adrenal; 2) a 37-year-old woman suffered from preeclampsia, persistent hypertension and orthostatic hypotension after a cesarean section. A diagnostic work-up revealed a catecholamine-secreting paraganglioma in the retroperitoneum. The patient underwent a laparosopic resection of the tumor; 3) a 27-year-old woman suffered from hypertension and episodes of palpitations, sweating, and dyspnea in the first trimester of her pregnancy. An ultrasound revealed a 5-cm mass in the left adrenal. She underwent a left adrenalectomy at the 17th week of pregnancy, which confirmed the diagnosis of pheochromocytoma; 4) a 34-year-old woman, at the 26th week of pregnancy, presented with an acute loss of vision and blood pressure of 230/140 mm Hg. Fundoscopy showed papilledema with soft exudates in both eyes. Chemical studies were positive and imaging revealed a left adrenal pheochromocytoma. Despite aggressive medical treatment, fetal distress mandated a laparotomy at the end of the 28th week of pregnancy. A healthy newborn was delivered and resection of the adrenal tumor confirmed the diagnosis of pheochromocytoma. CONCLUSIONS: Although rare, pheochromocytoma can cause severe peripartum hypertension. Screening for pheochromocytoma, ideally with plasma-free metanephrines, should be considered in cases of peripartum hypertension.

J Obstet Gynaecol Res. 2005 Dec;31(6):535-9.
Left atrial mechanical functions in pre-eclampsia.
Ingec M, Yilmaz M, Gundogdu F.
Department of Obstetrics and Gynecology, University of Ataturk, Erzurum, Turkey.

AIM: To assess the effect of short-term pressure overload on left atrial (LA) mechanical function in pre-eclampsia. METHODS: Twenty women with pre-eclampsia and 17 age-matched healthy pregnant women were included. LA volumes were measured echocardiographically at the time of mitral valve opening (Vmax), onset of atrial systole (p-wave at the electrocardiography = Vp) and mitral valve closure (Vmin) according to the biplane area-length method. RESULTS: The mean age, gestational age, weight and body surface area were similar in pre-eclampsia and controls. The ventricular septal and posterior wall thickness were greater in pre-eclampsia (P < 0.001). There were no significant differences in LA diameter, Vmax, Vmin, Vp, LA-passive emptying volume, LA-passive emptying fraction, LA-active emptying volume, LA-active emptying fraction, conduit volume, LA-total emptying volume and LA-total emptying fraction between the groups. CONCLUSION: Left atrial mechanical function didn't change in pre-eclampsia. We conclude that short-lasting pressure overload is not capable of inducing changes in LA function.

Am J Obstet Gynecol. 2000 Oct;183(4):911-3.
Validation of bioimpedance estimates of cardiac output in preeclampsia.
Scardo JA, Ellings J, Vermillion ST, Chauhan SP.
Spartanburg Regional Medical Center, Spartanburg, SC, USA.

OBJECTIVE: We sought to evaluate the capacity of a new thoracic electric bioimpedance system to estimate cardiac output in patients with preeclampsia. STUDY DESIGN: We performed a prospective comparison of thoracic electric bioimpedance and echocardiographic M-mode volumetric estimates of cardiac output (in liters per minute) in preeclampsia. Subjects with preeclampsia who were chosen by means of strict criteria (either a systolic blood pressure >/=140 mm Hg or a diastolic blood pressure 90 mm Hg, or both, and proteinuria >/=300 mg in 24 hours or >/=+1 on repeat dipstick measurement 6 hours apart) were asked to participate in an institutional review board-approved study. Thoracic electric bioimpedance and echocardiography were performed with the patients in the left lateral recumbent position. Thoracic electric bioimpedance estimates were recorded at bedside; investigators were blinded to 3 simultaneously obtained echocardiographic M-mode estimates of cardiac output. Means were entered as the estimate for each patient. To satisfy the assumption of independent samples, only 1 estimate from each technique was used for each patient. Data were analyzed by Bland-Altman comparison. Hemodynamic and demographic variables are presented as mean +/- SD. RESULTS: Fifteen patients were enrolled. Mean maternal age was 25.9 +/- 4.8 years, and mean gestational age was 34.0 +/- 3.5 weeks. Mean arterial pressure was 112 +/- 14 mm Hg. There was good agreement of thoracic electric bioimpedance-derived and M-mode-derived cardiac output estimates. CONCLUSIONS: In patients with preeclampsia, thoracic electric bioimpedance estimates of cardiac output compare well with echocardiographic M-mode estimates.

Obstet Gynecol. 1999 Nov;94(5 Pt 2):851.
L-transposition of the great arteries presenting as severe preeclampsia.
Harkness CB, Serfas DH, Imseis HM.
Department of Obstetrics and Gynecology, Mountain Area Health Education Center, and Asheville Cardiology Associates, North Carolina, USA.

Am Heart J. 1991 Jun;121(6 Pt 1):1768-75.
Left ventricular mechanics in preeclampsia.
Lang RM, Pridjian G, Feldman T, Neumann A, Lindheimer M, Borow KM.
Department of Medicine, University of Chicago Medical Center, IL 60637.

Increased systemic vascular resistance and contracted blood volume are characteristic findings in preeclampsia. These alterations in cardiovascular hemodynamics can adversely affect ejection phase indices of left ventricular performance making it difficult to separate abnormalities resulting from changes in load from those caused by depressed myocardial contractility. To address this issue the contractility-sensitive, load-independent relationship between left ventricular end-systolic wall stress and rate-corrected velocity of fiber shortening was assessed in 10 nulliparous patients with preeclampsia. Comparisons were made with data obtained from 10 age-matched normotensive women with uncomplicated pregnancies (control subjects). Studies were performed by means of two-dimensionally targeted M-mode echocardiography and calibrated carotid pulse tracings during early labor, 1 day after delivery, and 4 weeks after delivery. During early labor and 1 day after delivery, patients with preeclampsia had elevated blood pressure and increased total systemic resistance. These parameters returned to normal by 4 weeks after delivery. Before delivery and 24 hours after delivery, the patients with preeclampsia had lower overall left ventricular performance (as measured by cardiac output and rate-corrected velocity of fiber shortening) and higher left ventricular afterload (as measured by left ventricular end-systolic wall stress) when compared with control subjects. These differences were no longer present 4 weeks after delivery. Despite the time-related intergroup differences in hemodynamics, left ventricular contractility was similar between normotensive and preeclamptic subjects at all stages of the study. Thus when load is eliminated as a confounding variable, the decrements in overall left ventricular performance measured in patients with preeclampsia reflect a mechanically appropriate response to increased afterload rather than an abnormality in the ventricular contractile state.

Am J Obstet Gynecol. 1986 Apr;154(4):910-3.
Two-dimensional and M-mode echocardiographic findings in hypertensive pregnant women.
Sanchez RA, Glenny JE, Marco E, Voto LS, Lapidus AM, Iglesias GH, Moledo LV, Margulies M.

Two-dimensional and M-mode echocardiograms were obtained during the thirty-second week of gestation from 69 women classified as follows: group I, 22 normotensive primigravid women; group II, 16 primigravid women with pregnancy-induced hypertension; group III, 21 percent women with essential hypertension; and group IV, 10 normotensive nonpregnant control subjects. Systolic, diastolic, and mean arterial pressures were higher in groups II and III than in groups I and IV (p less than 0.001). Echocardiographic dimensions were significantly increased in group III compared with the other groups (p less than 0.01). No significant differences were observed among the other groups in the echocardiographic parameters or in the indices of ventricular performance studied. In echocardiographic studies, chronic hypertensive pregnant women are distinguished from patients with pregnancy-induced hypertension because the former have ventricular hypertrophy resulting from the pressure overload exerted for a long period of time. Our patients with essential hypertension experienced no changes in left ventricular performance because of the early stage of their hypertensive disease.

Am J Obstet Gynecol. 1986 Nov;155(5):994-9.
Echocardiographic left ventricular mass to differentiate chronic hypertension from preeclampsia during pregnancy.
Thompson JA, Hays PM, Sagar KB, Cruikshank DP.

In order to differentiate pregnancy-induced hypertension from chronic systemic hypertension, we measured left ventricular mass for comparison in each trimester of pregnancy in 11 normotensive patients and 14 patients with chronic hypertension and in the third trimester in 10 patients with pregnancy-induced hypertension. The mean left ventricular mass was comparably increased above normal in the patients with chronic hypertension in all three trimesters. In the third trimester in the normotensive women, left ventricular mass (147 +/- 12 gm) was similar to that of the group with pregnancy-induced hypertension (157 +/- 16 gm), whereas the group with chronic hypertension had an elevated left ventricular mass (238 +/- 39 gm) (p less than 0.01). However, three patients with chronic hypertension developed superimposed pregnancy-induced hypertension. We concluded that an elevated left ventricular mass during pregnancy is consistent with underlying chronic hypertension but does not rule out superimposed pregnancy-induced hypertension. A normal left ventricular mass in the third trimester of a hypertensive pregnancy is most consistent with pregnancy-induced hypertension.

Adams, E., and Finlayson, A.:
Familial Aspects of Preeclampsia and Hypertension in Pregnancy.
Lancet 2:1375 (Dec. 23), 1961.

Blood pressure studies were performed on relatives of primigravidae delivered in hospital in Aberdeen. The sisters of 146 preeclamptic patients had a higher incidence of preeclampsia or hypertension in their first pregnancy than did the sisters of 273 primigravidae witlhout preeclampsia or hypertension. In 87 mothers who had at least one daughter with eclampsia or hypertension in her first pregnancy the mean systolic and diastolic pressures were significantly higher than in the 149 mothers none of whose daughters developed hypertension in a first pregnancy. Siblings of 176 middle age women who had had preeclalmpsia or hypertension in the first pregnancy some 20 years earlier showed higher mean systolic and diastolic pressures, at all ages than siblings of 177 middle-aged women who had been normotensive throughout their first pregnancies. The findings suggest a strong familial tendency to preeclampsia and hypertension in pregnancy and support the hypothesis that preeclampsia does not cause hypertension in later life but develops more often in women with an inherited hypertensive tendency in whom the hypertension would later have become manifest anyway. SAGALL

Adams, E., and Mac Gillivray, I.:
Long-term Effect of Preeclampsia on Blood-pressure.
Lancet 2:1373 (Dec. 23), 1961.

A group of women between 35 and 50 years of age were examined in regard to their blood pressure. One hundred and ninety-seven were nulliparous and 334 had their first pregnancy at least 15 years prior to this studv. Of this latter group 149 had had preeclampsia durinig that pregnancy and 185 had been normotensive. It was found that the mean blood pressures of those who had had mild or severe preeclampsia were significantlv higher than those who had not suffered preeclamrpsia. Higher mean blood pressures were found in the nulliparous women. The findings were interpreted as supporting the views that preeclampsia is not a direct cause of hypertension in later life; that in some women diagnosed as having, mild preeclampsia the rise of blood pressure resulted from temporary unmasking during pregnancy of a hypertensive tendency than subsided after delivery but returned in later life. It was also suggested that the proportion of women with severe preeclampsia who have this hypertensive tendency is no greater than average. SAGALL

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