Gestational weight gain and blood pressure control in physiological pregnancy and pregnancy complicated by hypertension.

BACKGROUND: Obesity is a widely recognised risk factor for chronic and gestational hypertension. Influence of gestational weight gain on blood pressure control throughout the pregnancy is not well characterised. MATERIAL AND METHODS: Women in the third trimester of a singleton pregnancy were recruited to the study. Medical records were analysed and a special survey was conducted to obtain history on hypertensive disorders in pregnancy and weight changes during pregnancy. Blood pressure measurements were taken during the office visit in line with international guidelines. Relationships between gestational weight gain and maximal and office values of systolic and diastolic blood pressure values were analysed. RESULTS: Data of 90 women in normal pregnancy, 40 with gestational hypertension and 21 with chronic hypertension were analysed. Gestational weight gain was 11.9 ± 4.6 kg in the normal pregnancy group, 13.0 ± 5 kg in the gestational hypertension group and 10.6 ± 3.4 kg in the chronic hypertension group. Gestational weight gain positively correlated with both office (r = 0.48; p < 0.001) and maximal blood pressure values (r = 0.34; p = 0.004) in normal pregnancy and with maximal blood pressure values (r = 0.57; p = 0.02) in women with chronic hypertension. No correlation was observed between gestational weight gain and blood pressure values among women with gestational hypertension. CONCLUSION: In normal pregnancy and in women with chronic hypertension greater gestational weight gain is related to higher blood pressure values in the third trimester.

Downregulated expression of microRNAs associated with cardiac hypertrophy and fibrosis in physiological pregnancy and the association with echocardiographically-evaluated myocardial function.

The aim of the present study was to analyze the profiles of cardiac microRNAs (miRNAs/miRs) in healthy pregnant women and non-pregnant controls. A total of 61 healthy women >18 years of age with singleton pregnancies in the third trimester were compared with 19 non-pregnant controls. Specifically, expression of miRNAs associated with cardiac hypertrophy (miR-1, miR-17-5, miR-22, miR-34a, miR-124, miR-133a, miR-195, miR-199a-3p, miR-199b, miR-210, miR-222 and miR-1249) and miRNAs associated with cardiac hypertrophy and fibrosis (miR-15b, miR-21, miR-26a, miR-29-a, miR-29c, miR-30c, miR-101, miR-146a, miR-191, miR-208a-5p and miR-328) were analyzed and compared with echocardiographic examination results. Both groups had similar cardiac miRNA expression profiles, but differed in quantitative evaluation. Women in the third trimester of physiological pregnancy exhibited downregulation of certain profibrotic miRNAs (miR-21, miR-30c and miR-328), decreased expression of a hypertrophic and antimetabolic miRNAs (miR-146a), downregulation of an antifibrotic miRNA (miR-222), and downregulation of a hypertrophic miRNA (miR-195). In pregnant women, the indices of systolic function were associated with miR-195 expression, and an interplay between miR-17-5p and diastolic function was observed. While the profiles of cardiac miRNAs expressed in healthy pregnant women and healthy non-pregnant controls were similar, these two groups differed in terms of expression of specific miRNAs. In the third trimester of physiological pregnancy, a downregulation of miR-17-5p, miR-21, miR-30c, miR-146a, miR-195, miR-222 and miR-328 was observed. The differences in the association between echocardiographic indices with miRNAs in pregnant and non-pregnant women suggest that miRNAs regulate both the structure and function of the pregnant heart, influencing cardiac muscle thickness as well as systolic and diastolic function.

Rise in antifibrotic and decrease in profibrotic microRNA protect the heart against fibrosis during pregnancy: A preliminary study.

BACKGROUND: Physiological pregnancy is associated with volume overload. Unlike cardiac pathologies linked with volume overload, such as mitral or aortic regurgitation, pregnancy is thought to be unrelated to fibrosis of the heart. However, changes in the cardiac extracellular matrix during pregnancy remain poorly understood. OBJECTIVES: The aim of the study was to examine the expression of 11 microRNAs associated with cardiac fibrosis (miR-21, miR-26a, miR-26b-5p, miR-29b-3p, miR-29c-3p, miR-101a, miR-146a, miR-208a, miR-223 and miR-328) during pregnancy and to compare them with a healthy control group. MATERIAL AND METHODS: Six women in singleton pregnancy (30-36 weeks) and 6 non-pregnant women as a control group were included in the study. Each woman underwent an echocardiographic examination, and had blood pressure on both arms measured and a blood sample taken. MicroRNAs expression was analyzed using Custom TaqMan® Array MicroRNA Cards (Applied Biosystems, Foster City, USA). RESULTS: Median age of the pregnant women was 34 years (range 25-39 years) and of the control group 32 years (range 29-43 years). Median week of pregnancy was 34 years (range 31-36 years). Most of the examined microRNAs had a lower expression in the pregnancy group (fold change 1.0). CONCLUSIONS: In the 3rd trimester of physiological pregnancy, there is a 244% increase in expression of miR-101a and a decrease by 73% in expression of miR-328. Both of these changes can protect against fibrosis during volume overload occurring in physiological pregnancy.

Plasma heart-type fatty acid binding protein is superior to troponin and myoglobin for rapid risk stratification in acute pulmonary embolism.

BACKGROUND: Irreversible right ventricular (RV) failure with myocardial damage may precipitate fatal outcome in acute pulmonary embolism (APE). Cytoplasmic heart-type fatty acid binding protein (H-FABP) is a sensitive and specific biomarker of myocardial damage. We assessed which biomarker of myocardial damage or RV stretching is the most useful for short-term risk stratification in APE. METHODS: We analyzed 77 patients (51 F, 26 M) aged 65.3+/-16.0 years with confirmed APE. On admission, systemic blood pressure and transthoracic echocardiography (for RV overload) were recorded and plasma concentrations of myoglobin (Mb), cardiac troponin T (cTnT), N-terminal fragment of proBNP (NT-proBNP) and H-FABP were evaluated. RESULTS: Fifteen (19.5%) patients died and 24 (31.2%) experienced complicated clinical course (CCC)-death/thrombolysis/cardiopulmonary resuscitation/intravenous vasopressors. Hazard ratio analysis demonstrated that plasma H-FABP, Mb, cTnT and NT-proBNP concentrations predicted fatal outcome. When only APE-related deaths were considered, plasma H-FABP concentrations indicated fatal outcome. Multivariate hazard ratio analysis revealed H-FABP as the only 30-day mortality predictor (HR 1.02 CI 95% 1.01-1.05). CONCLUSIONS: H-FABP measured on admission is useful for short-term risk stratification in APE. It appears to be superior to cTnT, NT-proBNP and Mb in the prediction of 30-day APE-related mortality.

Does saddle embolism influence short-term prognosis in patients with acute pulmonary embolism?

BACKGROUND: In some patients with acute pulmonary embolism (APE) thrombi may lodge at the levels of the bifurcation of pulmonary trunk and extend into both main pulmonary arteries, forming so-called saddle embolism (SE). AIM: To assess the incidence of SE and whether it is associated with an increased risk of complicated clinical course. METHODS: We studied 150 consecutive patients (94 females, 56 males) aged 63.6+/-16.7 years with APE confirmed with contrast enhanced spiral computed tomography or transesophageal echocardiography. RESULTS: SE was detected in 22 (14.7%) patients. Mean age (SE vs N-SE) was 64.3+/-17.4 vs 63.5+/-16.6 years, heart rate 100.8+/-14.1 beats/min vs 97.8+/-21.1 beats/min, systolic blood pressure 126.2+/-20.1 vs 127.1+/-23.3 mmHg and blood pulsoximetry 92 (68-98) vs 91 (30-98) % (all differences NS). In patients with SE, echocardiographic signs of the right ventricular overload, defined as right to left ventricular end - diastolic ratio >0.6 with right ventricular hypokinesia and/or maximal tricuspid peak systolic gradient >30 mmHg with shortened acceleration time of pulmonary ejection <80 ms, were more frequent (77.3% vs 51.6%, p=0.04), as was the mid-systolic deceleration of pulmonary ejection velocity (77.3% vs 49.2%, p=0.04). Mortality and complicated clinical course rates were similar in patients with SE or N-SE (mortality: 4.5% vs 13.3%, NS, and complicated clinical course: 34.4% vs 25.0%, NS). CONCLUSIONS: Saddle pulmonary embolism is frequent, especially in patients with echocardiographic signs of impaired pulmonary ejection pattern. Saddle embolism does not indicate unfavourable clinical outcome and probably should not influence treatment selection.

Cardiac troponin T monitoring identifies high-risk group of normotensive patients with acute pulmonary embolism.

STUDY OBJECTIVES: Indications for thrombolysis in normotensive patients with pulmonary embolism (PE), based on the presence of right ventricular (RV) overload during transthoracic echocardiography (TTE), are controversial. We checked whether the monitoring of cardiac troponin T (cTnT) might help in risk stratification by detecting patients with RV myocardial injury. PATIENTS AND DESIGN: We studied 64 normotensive patients (30 women and 34 men) with a mean (+/- SD) age of 61.3 +/- 17 years and PE, who had undergone TTE for the assessment of RV overload. Plasma cTnT levels were measured quantitatively (detection limit, > 0.01 ng/mL) at hospital admission, and subsequently three times at 6-h intervals. Heparin therapy alone was used in 87.5% of patients, while 12.5% of patients received thrombolysis. RESULTS: cTnT was detected in 50% of patients. All eight in-hospital deaths occurred in the troponin-positive group, however, in one case the results of the first three assays had been negative. Elevated plasma cTnT increased the risk of PE-related death (odds ratio [OR], 21; 95% confidence interval [CI], 1.2 to 389). Increased age and elevated tricuspid regurgitant jet velocity, but not RV diameter/left ventricle diameter ratio, influenced the hospital mortality rate. Increased cTnT level was the only parameter predicting 15 in-hospital clinical adverse events (ie, death, thrombolysis, cardiopulmonary resuscitation, and IV use of catecholamine agents) [OR, 24.1; 95% CI, 2.9 to 200]. CONCLUSIONS: Patients with PE and elevated cTnT levels detected during repetitive assays are at a significant risk of a complicated clinical course and fatal outcome.

Myoglobin stratifies short-term risk in acute major pulmonary embolism.

BACKGROUND: Concentrations of cardiac troponins can be elevated in acute pulmonary embolism (APE) indicating myocardial injury. Although concentration of myoglobin (MYO) increases after myocardial damage, even before detectable rise of cardiac troponin levels occurs, MYO was not evaluated in APE. Therefore, we assessed prevalence and prognostic significance of myoglobin in major APE. METHODS: We studied 46 patients (30 women, aged 61.9+/-17.8 years) with major APE defined with right ventricular dilatation. On admission serum myoglobin, and cardiac troponin T (cTnT) were measured. Serum MYO concentrations >58 ng/ml for women, and >72 ng/ml for men were considered abnormal. CTnT>0.01 ng/ml was regarded to indicate myocardial injury. RESULTS: MYO levels exceeding sex specific norms were found in 21/46 (45.7%) of patients, while detectable cTnT was found in 24/46 (52.1%) of patients. Seven patients died during hospitalization. Elevated MYO significantly predicted in-hospital mortality (OR 25, 95% CI 1.3-474.2), while increased cTnT concentration did not affect the survival. Among clinical and echocardiographic variables only older age indicated worse prognosis (OR 1.6, 95% CI 1.06-2.41). CONCLUSIONS: Myoglobin levels are elevated in serum on admission in almost half of patients with major APE. Elevated myoglobin level, marker of myocardial injury, is a powerful predictor of increased risk of fatal outcome in major pulmonary embolism.

[Myocardial injury secondary to acute pulmonary embolism - a case report]. / Ostra zatorowosc plucna z objawami uszkodzenia miesnia sercowego.

A case of a 37-year-old male admitted to the hospital due to dyspnea and chest pain is presented. Electrocardiogram showed negative T waves in V1 and V2 as well as subtle ST segment elevation in all precordial leads. Cardiac enzymes were moderately elevated. The initial diagnosis was myocarditis or acute coronary syndrome, however, transthoracic echocardiography showed a marked right ventricular overload which suggested acute pulmonary embolism. The latter diagnosis was confirmed by transesophageal echocardiography which revealed thrombosis of both left and right pulmonary arteries. The patient received thrombolysis and anticoagulants, and his condition improved. He was discharged home and the course of a six-month follow-up was uneventful.

[Pulmonary embolism: a difficult diagnostic problem]. / Zatorowosc plucna--trudny problem diagnostyczny.

INTRODUCTION: The mortality of untreated pulmonary embolism (PE) is estimated at approximately 30% of patients, whereas treatment decreases it to 2-8%. A specific combination of symptoms present in PE may suggest other cardiac or lung disorder. OBJECTIVES: To evaluate frequencies of clinical symptoms and changes in diagnostic investigations misleading to the recognition of acute coronary syndrome (ACS) or lung diseases (Ld) in PE patients. PATIENTS AND METHODS: Retrospective analysis of 154 records of individuals with recognized PE allowed to divide patients into groups suggestive of ACS (min. 2 of: chest pain, ischemic changes on electrocardiogram (ECG) and elevated cardiac troponin T level [cTnT >0.01 ng/ml]) or suggestive of the Ld (min. 2 of: dyspnea, cough, fever, lung consolidations on chest radiograph). RESULTS: Fifty-five (36%) patients were classified to the ACS group and 54 (35%) to Ld group, while 69 (45%) patients were not included to either group. Twenty-four (16%) patients fulfilled criteria of both groups. There were no significant differences in the frequency of coronary heart disease, heart failure, atrial fibrillation and chronic obstructive pulmonary disease between groups. Elevated troponin level was observed in 68% of patients with chest pain and changes on ECG, and in 26% of patients without coexistence of these symptoms (p < 0.05). CONCLUSIONS: In most patients with final diagnosis of PE, symptoms and initial investigation results can mislead to the diagnosis of ACS or lung disease. The chest pain and ischemic changes on ECG are frequently associated with the myocardial injury resulting in increased troponin levels in PE patients.

Biomarker-based risk assessment model in acute pulmonary embolism.

AIMS: Despite growing interest in biomarkers application for risk evaluation in acute pulmonary embolism (APE), no decision-making levels have been defined. METHODS AND RESULTS: We developed a biomarker-based risk stratification in 100 consecutive, normotensive on admission, APE patients (35 males, 65 females, 62+/-18 years). On admission serum NT-proBNP and cardiac troponin T (cTnT) levels were assessed and echocardiography was performed. All-cause 40-day mortality was 15% and APE mortality was 8%. In univariable analysis, cTnT>0.07 microg/L predicted all-cause mortality, hazard ratio (HR) 9.2 (95% CI: 3.3-26.1, P<0.0001), and APE mortality, HR 18.1 (95% CI: 3.6-90.2, P=0.0004); similarly, NT-proBNP>7600 ng/L predicted all-cause and APE mortalities [HR 6.7 (95% CI: 2.4-19.0, P=0.0003) and 7.3 (95% CI: 1.7-30.6, P=0.007)]. NT-proBNP<600 ng/L indicated uncomplicated outcome. Multivariable analysis revealed that cTnT>0.07 microg/L was the most significant independent predictor, whereas NT-proBNP and systemic systolic blood pressure measured on admission and echocardiographic parameters were non-significant. APE mortality in patients with NT-proBNP> or =600 ng/L and cTnT> or =0.07 microg/L reached 33%. NT-proBNP<600 ng/L indicated group without deaths. APE mortality for patients with NT-proBNP> or =600 ng/L and cTnT<0.07 microg/L was 3.7%. Incorporation of echocardiographic data did not improve group selection. CONCLUSION: Simultaneous measurement of serum cTnT and NT-proBNP allows for precise APE prognosis. Normotensive patients on admission with cTnT> or =0.07 microg/L and NT-proBNP> or =600 ng/L are at high risk of APE mortality, whereas NTproBNP<600 ng/L indicates excellent prognosis.

[Electrocardiography and prediction of myocardial damage in patients with acute pulmonary embolism]. / Rola badania elektrokardiograficznego w ocenie uszkodzenia serca u chorych z ostra zatorowoscia plucna.

UNLABELLED: Acute pulmonary embolism (APE) may lead to myocardial necrosis detected by elevation of cardiac troponin levels. We tried to assess, if electrocardiographic abnormalities may help to define APE patients with myocardial damage and at high risk of complicated clinical course. Therefore we analyzed 50 patients (34F) aged 64.6 +/- 16.9 with confirmed APE. On admission 12-lead standard ECG was recorded and cardiac troponin T (cTnT) was determined quantitatively (Roche). Serum cTnT levels > 0.01 ng/ml, regarded to indicate myocardial injury, were detected in 29 (58%) patients. ST segment depression in ECG was found in 24% of all patients and was more frequent in cTnT + then in group without myocardial injury (41.4% vs 0%, p=0.004). Complicated clinical course and death in acute pulmonary embolism were also more frequently observed in group with ST segment depression (47.1% vs 12.1%, p = 0.03 and 75.0% vs 14.3%, p = 0.02 respectively). Although negative T waves were slightly more frequent in patients with elevated serum troponin T level (65.5% vs 42.9%) and in patients, who died of pulmonary embolism (62.5% vs 54.8%), the difference did not reach statistical significance. CONCLUSION: ST segment depression detected in standard ECG in patients with APE suggests myocardial injury and may indicate unfavourable clinical course.