Hypertension Of Unknown Cause Research Articles

Evaluation of Lipid Profile on Hypertensive Patients: An Observational Study from North Sulawesi, Indonesia

Hypertension is a major cause of premature death worldwide and a risk factor for cardiovascular disease (CVD). The prevalence of hypertension in Indonesia is 34.11%, and about 95% of hypertension in Indonesia is essential hypertension of unknown cause and multifactorial. Dyslipidemia is characterized by an increase or decrease in the lipid fraction in plasma. Patients with hypertension who are accompanied by dyslipidemia have a risk of 18.1 times more likely to develop coronary heart disease than those without dyslipidemia. This study aimed to determine the prevalence and relationship between lipid profile levels and blood pressures of hypertensive patients in North Sulawesi, Indonesia. This was a cross-sectional study conducted on 132 inpatients and outpatients with hypertension. Physical examinations including systolic and diastolic blood pressure (SBP, DBP) and body mass index (BMI) were performed. Fasting lipids including total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), triglycerides (TG), and high-density lipoprotein cholesterol (HDL-C) were evaluated. Overall, 79.5% of the subjects had dyslipidemia, and more prevalent in females and over 45 years of age. The most common type of dyslipidemia observed was hypercholesterolemia (51.5%), followed by high LDL-C (34.1%), elevated TG (31.8%), and low HDL-C (31.1%). There were statistically significant correlations found between lipid profiles and other cardiovascular risk factors only in females, namely a positive correlation between LDL-C and DBP and a negative correlation between HDL-C and age. As conclusion, the prevalence of dyslipidemia in this study was high. A statistically significant positive correlation between lipid profile and blood pressures was found only in females.

Prevalence of Primary Aldosteronism Across the Stages of Hypertension Based on a New Combined Overnight Test.

Primary aldosteronism (PA) is the most common endocrine cause of arterial hypertension. Despite the increasing incidence of hypertension worldwide, the true prevalence of PA in hypertension was only recently recognized. The objective of the work was to estimate the prevalence of PA in patients at different stages of hypertension based on a newly developed screening-diagnostic overnight test. This is a prospective study with hypertensive patients (n=265) at stage I (n=100), II (n=88), and III (n=77) of hypertension. A group of 103 patients with essential hypertension without PA was used as controls. PA diagnosis was based on a combined screening-diagnostic overnight test, the Dexamethasone-Captopril-Valsartan Test (DCVT) that evaluates aldosterone secretion after pharmaceutical blockade of angiotensin-II and adrenocorticotropic hormone. DCVT was performed in all participants independently of the basal aldosterone to renin ratio (ARR). The calculated upper normal limits for post-DCVT aldosterone levels [3 ng/dl (85 pmol/l)] and post-DCVT ARR [0.32 ng/dl/μU/ml (9 pmol/IU)] from controls, were applied together to establish PA diagnosis. Using these criteria PA was confirmed in 80 of 265 (30%) hypertensives. The prevalence of PA was: 21% (21/100) in stage I, 33% (29/88) in stage II, and 39% (30/77) in stage III. Serum K+ levels were negatively correlated and urinary K+ was positively correlated in PA patients with post-DCVT ARR (r=-0.349, p <0.01, and r=0.27, p <0.05 respectively). In conclusion, DCVT revealed that PA is a highly prevalent cause of hypertension. DCVT could be employed as a diagnostic tool in all subjects with arterial hypertension of unknown cause.

Unusual long survival in a case of heterotaxy and polysplenia

Heterotaxy syndrome with polysplenia is an extremely rare congenital disorder caused by a disruption in the embryonic development that results in an abnormal arrangement of the abdominal and thoracic organs. We present the case of a 59-year-old female patient with invasive ductal carcinoma of the right breast (luminal A type) and CT findings of heterotaxy syndrome with polysplenia. The most remarkable anomalies identified were a left inferior vena cava draining into the hemiazygos vein, absent inferior vena cava at the thoracic level, and hepatic veins directly draining into the right atrium. Moreover, an atrial septal defect was identified, explaining the pulmonary hypertension of unknown cause previously detected in the patient. The relevance of this case lies in the unusual anatomical abnormalities found and the large patient survival, having in to account the great rate of heterotaxy syndrome mortality in the first years of life.

Severe pulmonary hypertension due to combined pulmonary fibrosis and emphysema: another cause of death among smokers.

In 2005, the combined pulmonary fibrosis and emphysema (CPFE) was first defined as a distinct entity, which comprised centrilobular or paraseptal emphysema in the upper pulmonary lobes, and fibrosis in the lower lobes accompanied by reduced diffused capacity of the lungs for carbon monoxide (DLCO). Recently, the fibrosis associated with the connective tissue disease was also included in the diagnosis of CPFE, although the exposure to tobacco, coal, welding, agrochemical compounds, and tire manufacturing are the most frequent causative agents. This entity characteristically presents reduced DLCO with preserved lung volumes and severe pulmonary hypertension, which is not observed in emphysema and fibrosis alone. We present the case of a 63-year-old woman with a history of heavy tobacco smoking abuse, who developed progressive dyspnea, severe pulmonary hypertension, and cor pulmonale over a 2-year period. She attended the emergency facility several times complaining of worsening dyspnea that was treated as decompensate chronic obstructive pulmonary disease (COPD). The imaging examination showed paraseptal emphysema in the upper pulmonary lobes and fibrosis in the middle and lower lobes. The echo Doppler cardiogram revealed the dilation of the right cardiac chambers and pulmonary hypertension, which was confirmed by pulmonary trunk artery pressure measurement by catheterization. During this period, she was progressively restricted to the minimal activities of daily life and dependent on caregivers. She was brought to the hospital neurologically obtunded, presenting anasarca, and respiratory failure, which led her to death. The autopsy showed signs of pulmonary hypertension and findings of fibrosis and emphysema in the histological examination of the lungs. The authors highlight the importance of the recognition of this entity in case of COPD associated with severe pulmonary hypertension of unknown cause.

Use of Serum Vitamin B12 Level as a Marker to Differentiate Idiopathic Noncirrhotic Intrahepatic Portal Hypertension from Cryptogenic Cirrhosis

Idiopathic non-cirrhotic intrahepatic portal hypertension (NCIPH) is often mis-diagnosed as cryptogenic cirrhosis. Serum vitamin B12 levels can be raised in cirrhosis, probably because of excess release or reduced clearance. Because NCIPH is characterised by long periods of preserved liver function, we examined whether serum B12 level could be used as a marker to differentiate NCIPH from cryptogenic cirrhosis. We analysed serum B12 levels in 45 NCIPH and 43 cryptogenic cirrhosis patients from January 2009 to September 2011. Serum B12 levels were significantly lower in NCIPH patients than in cryptogenic cirrhosis patients (p < 0.001) and were useful in differentiating the two disorders (area under ROC: 0.84; 95% C.I: 0.76-0.93). Low serum B12 level (≤250 pg/ml) was noted in 25/72 (35%) healthy controls, 14/42 (33%) NCIPH patients, and 1/38 (3 %) cryptogenic cirrhosis patients. In patients with intrahepatic portal hypertension of unknown cause, serum B12 level ≤ 250 pg/ml was useful for diagnosing NCIPH (positive predictive value: 93 %, positive likelihood ratio 12.7), and serum B12 level >1,000 pg/ml was useful in ruling out NCIPH (negative predictive value: 86 %, negative likelihood ratio: 6.67). Low serum B12 levels (≤250 pg/ml) correlated with diagnosis of NCIPH after adjusting for possible confounders (O.R: 13.6; 95% C.I:1.5-126.2). Among patients in Child's class A, serum B12 level was ≤250 pg/ml in 14/35 NCIPH patients compared with 1/21 cryptogenic cirrhosis patients (O.R: 13.3; 95% C.I: 1.6-111). Serum vitamin B12 level seems to be a useful non-invasive marker for differentiation of NCIPH from cryptogenic cirrhosis.

Clinical Analysis of 15 Cases of Liver Nodular Regenerative Hyperplasia

Nodular regenerative hyperplasia (NRH) of liver may be one of the leading causes of non-cirrhotic intrahepatic portal hypertension (NCIPH), although the exact relationship is currently unknown. Diagnosis of NRH is relatively difficult and involves surgical pathology, and thus it is necessary to improve the preoperative recognition of NRH. Here, we analyze 15 cases of NRH to better understand this disease. All the liver specimens were microscopically examined by hematoxylin-eosin staining and reticulin and Masson trichrome staining. Diagnoses of NRH were confirmed by pathological examination. Clinically, NRH presents as diffused liver lesions with mildly increased liver enzymes. Portal hypertension is the most common clinical manifestation presenting prominently as splenomegaly, hypersplenism, and esophageal varices bleeding. NRH is often associated with autoimmune or collagen vascular diseases, and such patients often present with a variety of positive autoantibodies and increased erythrocyte sedimentation rate (ESR), Ig and γ %. Pathological examination of the liver showed diffuse small regenerative nodules without fibrous septa and obstructive portal venopathy. For those patients with portal hypertension of unknown cause and preserved liver function, especially, those combined with autoimmune diseases, NRH should be considered.

Pseudotumor cerebri.

Probable cases of pseudotumor cerebri were described more than a hundred years ago. A great deal of controversy existed regarding proper terminology and disease characterization. The clinical entity was doubtful before the routine use of ventriculography in the 1930s. Throughout history, many terms have been used, including serous meningitis, pseudotumor cerebri, otitic hydrocephalus, angioneurotic hydrocephalus, toxic hydrocephalus, meningeal hypertension, hypertensive meningeal hydrops, pseudoabscess, intracranial hypertension of unknown cause, papilledema of indeterminate etiology, intracranial pressure without brain tumor, benign intracranial hypertension, and idiopathic intracranial hypertension.

Congenital hypertrichosis, osteochondrodysplasia, and cardiomegaly: Cantú syndrome

Cantú syndrome (hypertrichosis, osteochondrodysplasia, cardiomegaly) is a rare condition, previously reported in 13 patients. We report on two additional patients with this disorder. One of the patients had pulmonary hypertension of unknown cause which was responsive to steroid therapy. She also had unusual, deep plantar creases, not reported previously in Cantú syndrome. Autosomal recessive inheritance has been suggested previously on the basis of sib recurrence in one family and consanguinity in another. We have performed a segregation analysis based on all reported families to date; the data indicate autosomal recessive inheritance is unlikely. A new dominant mutation or microdeletion syndrome are more likely possibilities, sib recurrence possibly representing gonadal mosaicism. Am. J. Med. Genet. 85:395–402, 1999. © 1999 Wiley-Liss, Inc.

Congenital hypertrichosis, osteochondrodysplasia, and cardiomegaly: Cant� syndrome

Cantú syndrome (hypertrichosis, osteochondrodysplasia, cardiomegaly) is a rare condition, previously reported in 13 patients. We report on two additional patients with this disorder. One of the patients had pulmonary hypertension of unknown cause which was responsive to steroid therapy. She also had unusual, deep plantar creases, not reported previously in Cantú syndrome. Autosomal recessive inheritance has been suggested previously on the basis of sib recurrence in one family and consanguinity in another. We have performed a segregation analysis based on all reported families to date; the data indicate autosomal recessive inheritance is unlikely. A new dominant mutation or microdeletion syndrome are more likely possibilities, sib recurrence possibly representing gonadal mosaicism.

Primary pulmonary hypertenson in pregnancy: A case report

Primary pulmonary hypertension is a rare, incurable, and progressive disease. When it is associated with pregnancy, the mortality rises to >50%. We report a patient who was diagnosed with severe pulmonary hypertension of unknown cause in the twenty-second week of gestation. She was treated with an oral calcium-channel blocker and low-molecular-weight heparin and underwent delivery by cesarean section with good maternal and fetal outcome. Patients with severe pulmonary hypertension should, however, avoid pregnancy because of the high mortality, although cases have been reported with positive outcome.

Pheochromocytoma Associated with Pregnancy: A Case Report

Pheochromocytoma Associated with Pregnancy: A Case Report

Hypertension in babies following discharge from a neonatal intensive care unit

Seventeen babies who developed hypertension (systolic BP greater than 113 mm Hg) after discharge from a neonatal intensive care unit were followed for a period ranging from 6 to 42 months. Five of the babies had an apparent cause for hypertension--one each had coarctation of the aorta, neuroblastoma, renal artery thrombosis, and two ureteropelvic junction obstruction. Umbilical artery catheters had been used in two additional babies. Ten of the babies had no obvious etiology for their hypertension. No prenatal, obstetrical or postnatal factor could be determined that predisposed these babies to hypertension. Sixteen of the babies were treated, 4 by surgical techniques and 12 by drugs--propranolol with or without chlorothiazide. All children treated medically were able to discontinue antihypertensives by 24 months of age. We conclude that follow-up of all babies discharged from the neonatal intensive care unit should include careful monitoring of blood pressure; that such infants may develop hypertension of unknown cause and that hypertension in this patient population is responsive to medication. Additional study is required to determine if babies discharged from neonatal intensive care units are at high risk for developing hypertension and to determine the natural history, prognosis and optimum treatment for the babies.

Contribution of lead to hypertension with renal impairment.

Hypertension of unknown cause is generally termed "essential." Because hypertension has long been considered a possible complication of lead poisoning and the EDTA lead-mobilization test has proved to be a sensitive indicator of excessive body stores of lead, we used this test to evaluate cumulative past lead absorption in 48 men diagnosed as having essential hypertension. Patients who had hypertension with reduced renal function (i.e., serum creatinine level greater than 1.5 mg per deciliter [133 mumols per liter]) had significantly larger amounts of mobilizable lead than did patients who had hypertension without renal impairment. The increase in mobilizable lead was not due to the renal disease itself, since 22 control patients without a history of essential hypertension but with comparable renal impairment from known causes excreted significantly less lead chelate during the three-day test. These data suggest that lead may have an etiologic role in the renal disease of some patients usually designated as having "essential" hypertension.

The role of hydralazine therapy for pulmonary arterial hypertension of unknown cause.

Hydralazine was administered acutely to 12 patients who had pulmonary arterial hypertension of unknown cause. All of the patients were studied at rest and nine during exercise. On the basis of hydralazine response at rest, the patients were divided in two groups. In six patients (group A), pulmonary arteriolar resistance (Rp) decreased from 8.4 +/- 1.4 to 4.8 +/- 1.4 U/m2 (p less than 0.001), cardiac index (CI) increased from 3.47 +/- 0.3 to 5.86 +/- 0.5 1/min/m2 (p less than 0.005) and systemic resistance (Rs) decreased from 25 +/- 4 to 14 +/- 2 U/m2 (p less than 0.01). The Rp/Rs ratio did not change significantly after hydralazine (0.32 +/- 0.03 vs 0.33 +/- 0.07, NS). In the other six patients (group B), Rs decreased from 25 +/- 2 to 17.0 +/- 1 U/m2 (p less than 0.01), but the other variables did not change significantly. Our results suggest that the pulmonary vasodilatory effect of hydralazine caused a marked reduction in right ventricular afterload in group A. In group B, a marked systemic vasodilatory effect occurred and right ventricular afterload was not reduced. On the basis of the previous hemodynamic response, only group A patients were treated with oral hydralazine (50 mg every 6 hours). Hemodynamic measurements were repeated 48 hours after hydralazine, both at rest and during exercise, as well as 8 months later in five of the six patients in whom the beneficial hemodynamic effects persisted. These data suggest that hydralazine can reduce Rp in selected patients (pulmonary arterial pressure less than 60 mm Hg, Rp less than 15 U/m2 and Rp/Rs ratio less than 0.7) with pulmonary hypertension of unknown cause.

Congenital abnormalities associated with extrahepatic portal hypertension.

Congenital abnormalities were present in 12 out of 30 (40%) children with extrahepatic portal hypertension of unknown cause, but in only 2 out of 17 (12%) children with extnahepatic portal hypertension secondary to umbilical vein catheterization or omphalitis. The most frequent abnormalities in this series and in published reports were atrial septal defect, malformation of the biliary tract, and anomalous inferior vena cava. These findings are consistent with the view that some cases with extrahepatic portal hypertension are congenital in origin.

Persistent fetal circulation: Newly recognized structural features.

Three infants died with pulmonary hypertension of unknown cause during the first three months of life. Their lungs were examined using quantitative morphologic techniques. In all three cases the intra-acinar pulmonary arteries were more muscular than normal, as shown both by an increase in thickness of the muscle coat in arteries which are normally muscular, and by extension of muscle into smaller and more peripheral intra-acinar arteries not normally muscular at this age. It is suggested that "persistent pulmonary hypertension" of the newborn infant is, in some infants, due to a structural abnormality of the pulmonary circulation which is present at birth.

Resistance to drainage of cerebrospinal fluid: clinical measurement and significance.

By infusing saline intrathecally at a constant rate until a new steady-state cerebrospinal fluid (CSF) pressure is attained, one can estimate clinically the apparent resistance (Ra) to drainage of CSF in mm saline/ml./minute. This intrathecal saline infusion test (ITSIT) was performed 36 times on 29 patients with diverse intracranial problems, and the results were analysed and, in most cases, compared with the pneumoencephalogram and the isotope cisternogram. The ITSIT is a safe, simple test to estimate Ra, but factors which are difficult to control (occult leaks from the subarachnoid space; independent fluctuations of CSF pressure) limit its reliability and clinical usefulness. If closely correlated with the clinical syndrome, the pneumoencephalogram, and the isotope cisternogram, an ITSIT may identify decisively the patient who needs a shunt. In addition the ITSIT offers another method by which to investigate the pathophysiological mechanisms of the various states of intracranial hypertension. Results from the test performed on four patients with intracranial hypertension of unknown cause (pseudotumor cerebri) suggest that the underlying mechanism in this condition is probably an impediment to normal CSF drainage.

Hyperdynamic ß-Adrenergic Circulatory State

Hemodynamic and pharmacological characteristics of 14 patients with clinical findings suggesting hyperdynamic β-adrenergic circulatory state (including 12 with hypertension of unknown cause) were compared with 13 essential hypertensive patients and 25 normotensive volunteer subjects. Patients with cardiac symptoms had significantly higher resting cardiac index and heart rate than normotensive or asymptomatic hypertensive individuals. Graded isoproterenol hydrochloride infusion increased heart rate significantly more in the symptomatic group than in the others, indicating increased β-receptor hyperresponsiveness. In nine of the 14 patients, isoproterenol produced an hysterical outburst, almost uncontrollable, which was promptly reversed with propranolol hydrochloride but not placebo. It therefore seems reasonable to ascribe the syndrome of cardiac awareness, increased heart rate responsiveness to various stimuli, and hyperkinetic circulation to increased β-adrenergic receptor reactivity. This conclusion is supported by remission of symptoms and reduction of arterial pressure with propranolol in all treated patients.

Effect of acetylcholine on pulmonary vascular resistance in a patient with idiopathic pulmonary hypertension.

Necropsy studies in cases of pulmonary hypertension of unknown cause show structural changes in the pulmonary vessels that are called irreversible. Acetylcholine chloride was infused at a rate of 2 mg. per minute into the outflow tract of the right ventricle of a 48-year-old woman who had pulmonary hypertension. The mean pulmonary artery pressure decreased from 56 to 25 mm. Hg and the pulmonary flow increased slightly. These findings are consistent with the theory that so-called idiopathic pulmonary hypertension may at some stage be maintained by vasoconstriction.

RECENT ADVANCES IN THE PATHOGENESIS AND TREATMENT OF ESSENTIAL HYPERTENSION

Article1 August 1949RECENT ADVANCES IN THE PATHOGENESIS AND TREATMENT OF ESSENTIAL HYPERTENSIONG. E. WAKERLIN, Ph.D., M.D., F.A.C.P.G. E. WAKERLIN, Ph.D., M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-31-2-312 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptBy essential hypertension, of course, is meant chronic hypertension of unknown cause. Approximately 90 per cent of all hypertensions seen clinically belong to this group. The hypertensions of known causes include those associated with nephritis, pyelonephritis, renal anomalies, renal tumors, pheochromocytomas, adrenal cortical tumors, pituitary basophilism, coarctation of the aorta, and certain lesions of the central nervous system. The exact mechanism of the increase in arterial blood pressure in even this latter group, however, is definitely known only in the case of pheochromocytomas; viz., an increased secretion of epinephrine. Nevertheless, clinical differentiation of these hypertensions from essential hypertension is vitally...References GOLDRINGCHASIS WH: Hypertension and hypertensive disease, 1944, Commonwealth Fund, Oxford Press. Google Scholar PAGECORCORAN IHAC: Arterial hypertension, 1945, Year Book Publishers, Chicago. Google Scholar BRAUN-MENENDEZ E (translated by L. DEXTER): Renal hypertension, 1946, C. C. Thomas, Springfield. Google Scholar Transactions of the First Conference on Factors Regulating Blood Pressure, Josiah Macy, Jr. Foundation, April 24-25, 1947, New York, N. Y. Google Scholar Transactions of the Second Conference on Factors Regulating Blood Pressure, Josiah Macy, Jr. Foundation, January 8-9, 1948, New York, N. Y. (in press). Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Chicago, Illinois*Received for publication October 30, 1948.From the Department of Physiology, University of Illinois College of Medicine, Chicago, Illinois. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byDie Sympathektomie beim Hochdruck und ihre Ergebnisse 1 August 1949Volume 31, Issue 2Page: 312-318KeywordsAortaBlood pressureCentral nervous systemEpinephrineHypertensionLesionsNephritisPathogenesisPheochromocytomaPyelonephritis ePublished: 1 December 2008 Issue Published: 1 August 1949 PDF downloadLoading ...