Systemic Hypertension In Dogs Research Articles

Thoracic and abdominal aortic alterations in dogs affected with systemic hypertension

Aortic remodeling is the consequence of untreated systemic hypertension along with aortic dilatation as a marker for target organ damage in human literature. Therefore, the present study was planned to detect the changes in aorta at the level of aortic root via echocardiography, thoracic descending aorta via radiography and abdominal aorta via ultrasonography in healthy (n = 46), diseased normotensive (n = 20) and systemically hypertensive dogs (n = 60). The aortic root dimensions were measured at the level of aortic annulus, sinus of valsalva, sino-tubular junction and proximal ascending aorta via left ventricular outflow tract view of echocardiography. The thoracic descending aorta was subjectively assessed for any disparity in size and shape of aorta via lateral and dorso-ventral view of chest radiography. The abdominal aorta was assessed via left and right paralumbar window for calculating the aortic elasticity along with aortic and caudal venacaval dimensions to calculate the aortic-caval ratio. The aortic root measurements were dilated (p < 0.001) in systemically hypertensive dogs with a positive correlation (p < 0.001) with systolic blood pressure (BP). Thoracic descending aorta was also (p < 0.05) altered in the size and shape (undulation) of systemically hypertensive dogs. Abdominal aorta was markedly stiffened with reduced elasticity (p < 0.05) along with dilatation (p < 0.01) in hypertensive dogs. Also, there was a positive correlation (p < 0.001) of aortic diameters and aortic-caval ratio and negative correlation (p < 0.001) of aortic elasticity with systolic BP. Therefore, it was concluded that aorta could be considered as an important target organ damage of systemic hypertension in dogs.

Retrospective evaluation of systemic hypertension in dogs with nonassociative (primary) immune-mediated hemolytic anemia (December 2016 to April 2019): 26 cases.

To report the prevalence of arterial hypertension in a population of dogs with nonassociative immune-mediated hemolytic anemia (IMHA) on presentation and during hospitalization. To determine the relationships of systolic blood pressure (SBP) with mortality and a prognostic indicator, the canine hemolytic anemia objective score. Retrospective observational study (December 2016 to April 2019). University teaching hospital. Twenty-six clinical dogs presenting to the ICU with nonassociative (primary) IMHA and a control group of 23 clinical dogs with idiopathic epilepsy hospitalized in the ICU for seizure treatment or monitoring. None. Hypertension was defined as SBP≥160mm Hg and severe hypertension as SBP≥180mm Hg. Mean SBP was significantly increased in IMHA dogs (161mm Hg, SD=21) compared to ICU control dogs (138mm Hg, SD=14; P<0.005). Hypertension was present in 13 of 26 (50.0%) dogs across the period of hospitalization and was severe in three of 26 (11.5%). During at least 1 day of hospitalization, 18 of 26 (69.2%) dogs were hypertensive and eight of 26 (34.6%) were severely hypertensive. Hypertension was not associated with short-term mortality or canine hemolytic anemia objective score. In this retrospective study, hypertension was more prevalent in dogs with nonassociative IMHA than a control population of ICU-hospitalized dogs. An association between autoimmune conditions and hypertension has been previously reported in people but not within a canine population. Hypertension in dogs may have an inflammatory or autoimmune etiology. SBP should be monitored closely in canine IMHA, in case antihypertensive treatment is required.

Echocardiographic changes in the shape and size of the aortic cusps in dogs with confirmed systemic hypertension.

Systemic hypertension (SH) in dogs typically occurs secondary to renal disease, diabetes mellitus, hyperadrenocorticism, malignant adrenal tumors, or various medications. Echocardiography performed on people with SH has shown asymmetric dilation of the sinuses at the level of the aortic valves, previously undescribed in canine patients. The objective of this retrospective case-control study was to determine if there was a difference in size and shape of the aortic cusps at the level of the sinus of Valsalva in dogs with SH compared to dogs with normal blood pressure. We reviewed echocardiographic findings in 74 dogs with SH and 37 dogs with normal blood pressure (NBP), defined as less than 150mmHg. Systemic hypertension was classified as mild (150-159mm Hg), moderate (160-179mm Hg), or severe (greater than 180mm Hg). There was a significant difference (P<.001) in the mean size of the aorta cusps at the level of the sinuses in 67 of 74 dogs with SH and none of 37 dogs with NBP. Of the 74 dogs with SH, 70 had left ventricular hypertrophy (18 asymmetric, 15 concentric, and 37 eccentric). Additionally, there was aortic root dilatation in 15 dogs, aortic insufficiency in 21, mitral regurgitation in 50, and left atrial enlargement in 71. The standard deviation of the three cusp measurements between the dogs with SH and dogs with NBP had a sensitivity of 92% and specificity of 97% for diagnosis of SH. Asymmetric size of the aortic cusps on echocardiography is therefore a reliable indicator of SH in dogs.

Erratum for Prevalence and risk factors associated with systemic hypertension in dogs with spontaneous hyperadrenocorticism.

Erratum for Prevalence and risk factors associated with systemic hypertension in dogs with spontaneous hyperadrenocorticism.

ACVIM consensus statement: Guidelines for the identification, evaluation, and management of systemic hypertension in dogs and cats

An update to the 2007 American College of Veterinary Internal Medicine (ACVIM) consensus statement on the identification, evaluation, and management of systemic hypertension in dogs and cats was presented at the 2017 ACVIM Forum in National Harbor, MD. The updated consensus statement is presented here. The consensus statement aims to provide guidance on appropriate diagnosis and treatment of hypertension in dogs and cats.

Prevalence and risk factors associated with systemic hypertension in dogs with spontaneous hyperadrenocorticism.

BackgroundSystemic hypertension (SH) is common in dogs with hyperadrenocorticism (HAC) however there are not many studies assessing its prevalence and risk factors.ObjectivesTo determine the prevalence and severity of SH in dogs with HAC and its association with clinical and laboratory findings to identify potential risk factors.AnimalsSixty‐six client owned dogs with spontaneous HAC.MethodsRetrospective cross‐sectional study. Medical records of dogs with HAC were reviewed. Systolic blood pressure (SBP) was measured using Doppler ultrasonography. Clinical signs, physical examination findings and clinicopathologic data (CBC, serum biochemistry and electrolytes, urinalysis and urinary culture, and adrenal function tests) were reviewed for analysis.ResultsPrevalence of SH (≥150 mm Hg) was 82% (54/66) and prevalence of severe SH (≥180 mm Hg) was 46% (30/66). All dogs with thrombocytosis had SH (P = .002), and a platelet count ≥438 × 103/μL was 100% specific and 61.1% sensitive to predict SH (AUC = .802, P = .001). Median potassium levels were lower in hypertensive dogs (4.1 mEq/L, range 3.1‐5.4 mEq/L) than in normotensive ones (4.5 mEq/L, range 4.0‐5.0 mEq/L) (P = .007). Dogs with UPC ≥ 0.5 had higher median SBP than those without proteinuria (P = .03). Dogs with concurrent diabetes mellitus seemed to have a reduced risk of SH (OR = .118, 95%CI = .022‐.626, P = .02).Conclusions and Clinical ImportanceSystemic hypertension is common in dogs with HAC and is frequently severe. Blood pressure should be routinely assessed in these dogs, especially if thrombocytosis, proteinuria or low potassium concentrations are present.

Aortic to caudal vena cava ratio measurements using abdominal ultrasound are increased in dogs with confirmed systemic hypertension.

Chronically sustained systemic hypertension in dogs can damage the kidneys, eye, brain, heart, and vessels. In human medicine, systemic hypertension has been implicated as the most common risk factor for aorta dilation, which can progress to an aneurysm. Abdominal ultrasound has been commonly used to monitor the size of the abdominal aorta in people with systemic hypertension. In this retrospective cross-sectional abdominal ultrasound study, evaluation of the size of the abdominal aorta relative to the caudal vena cava was performed in 18 control dogs and 128 dogs with confirmed systemic hypertension. Preexisting conditions contributing to systemic hypertension in these dogs were renal disease, hyperadrenocorticism, diabetes mellitus, adrenal tumors, and previous administration of phenylpropanolamine or palladia. The abdominal aorta and caudal vena cava were assessed from longitudinal images cranial to the trifurcation with measurements made from outer border to outer border of the walls, being careful not to compress the caudal vena cava that would alter its size. Our hypothesis was the ratio of the diameter of the abdominal aorta to caudal vena cava would be higher in dogs with systemic hypertension compared to dogs with normal blood pressure. The mean abdominal aorta-caudal vena cava ratio was 1.028 in control dogs with a normal blood pressure and 1.515 in dogs with systemic hypertension. In dogs with confirmed systemic hypertension, the abdominal aorta was dilated compared to the caudal vena cava in the caudal abdomen. An increase in the abdominal aorta-caudal vena cava ratio in a dog should raise suspicion for the presence of systemic hypertension and prompt evaluation of blood pressure.

ACVIM consensus statement: Guidelines for the identification, evaluation, and management of systemic hypertension in dogs and cats.

An update to the 2007 American College of Veterinary Internal Medicine (ACVIM) consensus statement on the identification, evaluation, and management of systemic hypertension in dogs and cats was presented at the 2017 ACVIM Forum in National Harbor, MD. The updated consensus statement is presented here. The consensus statement aims to provide guidance on appropriate diagnosis and treatment of hypertension in dogs and cats.

Cardiovascular changes in a dog with a secondary systemic hypertension chronic renal failure: case report

Systemic hypertension in dogs can occur secondary to chronic kidney disease (CKD), because there is activation of the renin angiotensin aldosterone system (RAAS) leading to vasoconstriction and increased blood pressure and afterload, promoting concentric hypertrophy of the ventricular myocardium . The objective of this study is to report the radiographic, electrocardiographic and Doppler echocardiographic a dog carrier hypertension secondary to CKD before and after therapy. We treated a canine patient with CKD presenting unilateral ocular hemorrhagic stroke and presence of mitral murmur grade II / VI. Laboratory tests revealed renal azotemia, with urinalysis showing isosthenuria, proteinuria and granular cylinders. Blood pressure (SBP) showed average values ​​of 250 mmHg. On the chest radiograph Vertebral Heart System (VHS) was 10.7 vertebrae, indicating cardiomegaly and increased left ventricular (LV), as suggested in electrocardiography with increasing duration of QRS Complex. Doppler echocardiography showed hypertrophic cardiomyopathy and decrease in LV internal diâmentro, ventricular septal hypertrophy, dilatation of the aorta and increased fractional shortening (% FEC) LV. Therapy was instituted the basis of enalapril maleate and commercial diet for CKD. After 90 days, there was a reduction in ocular hemorrhagic stroke, with mean SBP maintaining the 130mmHg, reduction in serum biochemical values ​​in VHS (10.6 v) heart in myocardial hypertrophy and LV% FEC. The changes found suggest myocardial remodeling due to hypertension secondary source to CKD, with improvement after therapy instituted.

Occurrence of systemic hypertension in dogs with acute kidney injury and treatment with amlodipine besylate

To describe the occurrence of systemic hypertension in dogs with acute kidney injury and the efficacy of amlodipine besylate for its treatment. This retrospective study included 52 dogs with acute kidney injury (2007 to 2008) grouped based on the use of amlodipine in their treatment. Systemic blood pressure was measured with an oscillometric device at admission, before, during, and after amlodipine therapy. Occurrence of systolic systemic hypertension (≥160 mmHg) and severe systolic systemic hypertension (≥180 mmHg) was 37% and 15% at admission and increased with hospitalisation to 81% and 62%, respectively. Twenty-two dogs were treated with amlodipine, at a median daily dosage of 0·38 mg/kg (interquartile range 0·28 to 0·49) divided in one to two applications per day. Amlodipine therapy was associated with a decrease in systolic systemic blood pressure of 24 mmHg (12 to 34) and a correction of severe systemic hypertension in 10 of 11 dogs within 24 hours. Overall, 73% of the dogs survived with a significantly lower proportion of survivors in treated compared to non-treated dogs (59% versus 83%, respectively, P=0·05). Results of this study reveal that systemic hypertension is common in canine acute kidney injury and that treatment with amlodipine is beneficial in reducing systemic hypertension. The potential effect of amlodipine on global outcome requires prospective assessment.

Ocular lesions associated with systemic hypertension in dogs: 65 cases (2005–2007)

To characterize ocular findings in hypertensive dogs, determine prevalence of hypertension in dogs with ocular disease suggestive of hypertension, and examine possible relationships between degree of hypertension and ocular disease. Retrospective case series. 65 dogs initially referred for blood pressure measurement (n = 22), ophthalmic examination (25), or both (18). Medical records were reviewed to identify dogs examined at the teaching hospital that underwent a complete ophthalmic examination and blood pressure measurement within a 24-hour period between January 1, 2005, and December 31, 2007. Signalment, history, blood pressure measurements, ophthalmic examination findings, and any vasoactive drug treatments were recorded. Ocular lesions considered likely to be associated with systemic hypertension included retinal hemorrhage, retinal detachment, hyphema, tortuous vessels, and subretinal edema. Of the 65 dogs, 42 were hypertensive (systolic blood pressure ≥ 160 mm Hg) and 23 were normotensive. Sixty-two percent (26/42) of hypertensive dogs had ≥ 1 type of ocular lesion identified. Retinal hemorrhage was the most common ocular lesion in hypertensive dogs (17/42 [40%]). The presence of ≥ 1 type of ocular lesion had moderate sensitivity and specificity of 62% and 61 %, respectively, for identification of hypertension. Fifteen of the 25 (60%) dogs referred for blood pressure measurement after initial ophthalmic examination were found to be hypertensive. Ocular lesions are common in dogs with systemic hypertension. Dogs with hypertension or diseases associated with hypertension should be monitored carefully for evidence of ocular target organ damage, and hypertension should be systematically ruled out in dogs with characteristic ocular lesions.

Guidelines for the Identification, Evaluation, and Management of Systemic Hypertension in Dogs and Cats

Guidelines for the Identification, Evaluation, and Management of Systemic Hypertension in Dogs and Cats

Guidelines for the Identification, Evaluation, and Management of Systemic Hypertension in Dogs and Cats

Consensus Statements of the American College of Veterinary Internal Medicine (ACVIM) provide veterinarians with guidelines regarding the pathophysiology, diagnosis, or treatment of animal diseases. The foundation of the Consensus Statement is evidence‐based medicine, but if such evidence is conflicting or lacking, the panel provides interpretive recommendations on the basis of their collective expertise. The Consensus Statement is intended to be a guide for veterinarians, but it is not a statement of standard of care or a substitute for clinical judgment. Topics of statements and panel members to draft the statements are selected by the Board of Regents with input from the general membership. A draft prepared and input from Diplomates is solicited at the ACVIM Forum and via the ACVIM Web site and incorporated in a final version. This Consensus Statement was approved by the Board of Regents of the ACVIM before publication.

Guidelines for the Identification, Evaluation, and Management of Systemic Hypertension in Dogs and Cats

Consensus Statements of the American College of Veterinary Internal Medicine (ACVIM) provide veterinarians with guidelines regarding the pathophysiology, diagnosis, or treatment of animal diseases. The foundation of the Consensus Statement is evidence-based medicine, but if such evidence is conflicting or lacking, the panel provides interpretive recommendations on the basis of their collective expertise. The Consensus Statement is intended to be a guide for veterinarians, but it is not a statement of standard of care or a substitute for clinical judgment. Topics of statements and panel members to draft the statements are selected by the Board of Regents with input from the general membership. A draft prepared and input from Diplomates is solicited at the ACVIM Forum and via the ACVIM Web site and incorporated in a final version. This Consensus Statement was approved by the Board of Regents of the ACVIM before publication.

Systemic Hypertension in Dogs with Leishmaniasis: Prevalence and Clinical Consequences

A prospective study was performed (November 1998 to December 2003) to determine the prevalence of systemic hypertension (SH) in dogs with glomerular disease secondary to leishmaniasis. One hundred and five dogs with leishmaniasis were screened and staged for the presence of renal disease (RD) and SH. For the purpose of the study, RD was defined as serum creatinine concentration ≥ 1.4 mg/dL, a urine protein/creatinine ratio ≥ 0.5, or both. SH was defined as a systolic blood pressure (SBP) ≥ 180 mm Hg or an SBP between 150 and 179 mm Hg in the presence of clinical manifestations of SH. Fifty‐two (49.5%) of the dogs had some degree of RD, and 32 (61.5%) of these dogs were diagnosed with SH. Moreover, SH also was diagnosed in 3 dogs without RD. Left ventricular hypertrophy (LVH), estimated by echocardiography, was the most frequently observed systemic consequence of hypertension, being present in 32 (91.4%) of the hypertensive dogs. Echocardiographic abnormalities were not detected in any of the 33 dogs with leishmaniasis without RD, which were used as controls. Ocular consequences of SH were observed in only 2 (5.7%) of the dogs with hypertension. We conclude that SH is prevalent in dogs with RD secondary to leishmaniasis, not only in the more severe stages but also in the early course of the illness before azotemia becomes apparent. Canine leishmaniasis may be a useful natural model to study SH secondary to glomerular disease.

Systemic Hypertension in Dogs with Leishmaniasis: Prevalence and Clinical Consequences

A prospective study was performed (November 1998 to December 2003) to determine the prevalence of systemic hypertension (SH) in dogs with glomerular disease secondary to leishmaniasis. One hundred and five dogs with leishmaniasis were screened and staged for the presence of renal disease (RD) and SH. For the purpose of the study, RD was defined as serum creatinine concentration > or = 1.4 mg/dL, a urine protein/creatinine ratio > or = 0.5, or both. SH was defined as a systolic blood pressure (SBP) > or =180 mm Hg or an SBP between 150 and 179 mm Hg in the presence of clinical manifestations of SH. Fifty-two (49.5%) of the dogs had some degree of RD, and 32 (61.5%) of these dogs were diagnosed with SH. Moreover, SH also was diagnosed in 3 dogs without RD. Left ventricular hypertrophy (LVH), estimated by echocardiography, was the most frequently observed systemic consequence of hypertension, being present in 32 (91.4%) of the hypertensive dogs. Echocardiographic abnormalities were not detected in any of the 33 dogs with leishmaniasis without RD, which were used as controls. Ocular consequences of SH were observed in only 2 (5.7%) of the dogs with hypertension. We conclude that SH is prevalent in dogs with RD secondary to leishmaniasis, not only in the more severe stages but also in the early course of the illness before azotemia becomes apparent. Canine leishmaniasis may be a useful natural model to study SH secondary to glomerular disease.

Chronically increased intra-abdominal pressure produces systemic hypertension in dogs.

Determine if increased intra-abdominal pressure (IAP) alone can cause systemic hypertension in a chronic canine model. Evaluate effects of increase in IAP with progressive inflation and deflation of an intra-abdominal balloon on systemic blood pressure in experimental and control animals. Male dogs weighing 15-25 kg underwent placement of an intra-abdominal balloon which was progressively inflated on a weekly basis in the experimental animals (5) over 4 weeks to 25 mmHg above baseline and kept there for an additional 2 weeks before gradual deflation over 2 weeks. Control animals (5) had the balloon placed but not inflated. Pain was controlled with osmotic analgesic pumps. The animals were anesthetized, blood pressure (BP) measured and blood drawn for plasma renin activity (PRA), aldosterone, atrial naturetic peptide (ANP), catecholamines, and serum sodium (Na). A right heart catheter was inserted for measuring cardiac output (CO) and pulmonary artery occlusion pressure (PAOP) at baseline, week 5 (maximal IAP) and week 7 (after balloon deflation). The animals were weighed and urinary bladder pressures recorded weekly before and after abdominal balloon inflation. Systolic (122+/-3 to 155+/-5 mmHg, P<0.05) and diastolic (82+/-4 mmHg to 107+/-7 mmHg, P<0.05) BP rose at 5 weeks at 25 mmHg IAP>baseline and returned to control with balloon deflation. Both systolic and diastolic BP rose (P<0.05) above control animals BP at 15 mmHg IAP at 2 weeks and remained elevated until abdominal decompression, at week 7. There were no significant changes in net animal weight, PRA, aldosterone, ANF, catecholamines, Na, CO or PAOP. Increased IAP from progressively inflating an intra-abdominal balloon in dogs was associated with significant increases in systolic and diastolic BP that resolved with balloon deflation. Increased IAP may be a cause for systemic hypertension in central obesity and pre-eclampsia.

Aortic thrombosis as a cause of hypertension: an arteriographic study.

Goldblatt and his co-workers (1) discovered that constriction of one renal artery caused transient systemic hypertension in dogs and prolonged hypertension in other animals. Complete occlution of the renal artery did not produce this effect. Constriction of both renal arteries resulted in persistent hypertension, as did constriction of one renal artery after removal of the opposite kidney. It was also shown that hypertension could be produced by constricting the aorta proximal to the renal arteries but not by compression applied distal to these vessels. Excision of the ischemic kidney following unilateral constriction resulted in disappearance of the hypertension. Since these classical experiments, many cases of hypertension associated with constriction of a main renal artery have been reported. Among these a variety of arterial lesions has been found; all appear to have in common partial interruption of the blood flow to a kidney. These cases represent the human counterpart of Goldblatt's animal experiments. Yuile (2) classified constriction of the renal artery as of intrinsic and extrinsic origin. The intrinsic causes include embolism (3–7), thrombosis (8–12), developmental defects (13), aneurysm (14, 15), arteriosclerotic plaques (16), and syphilitic arteritis (17). Extrinsic causes are compression of the renal artery by aortic aneurysm (18), retroperitoneal tumor (19), hydatid cyst (20), organizing hematoma (21), intrarenal tumor (22), and kinking or torsion (23, 24). While the value of abdominal arteriography for the detection of these conditions has frequently been mentioned, relatively few arteriograms have been made for this purpose. In fact, there has been little effort to assess the status of the renal arteries by this means in any group of patients with hypertension, whatever the cause. In earlier reports on abdominal arteriography from the Cincinnati General Hospital (25, 26) only one of the 75 patients with hypertension showed constriction of a main renal artery. Because of this experience, we believe that arteriography has little value as a routine measure in the clinical investigation of the hypertensive patient. Moderately elevated blood pressure is not uncommon among patients suffering from thrombosis of the abdominal aorta. The explanation for this is obscure, but it is apparent from our own arteriograms and those appearing in the literature that it does not usually originate from renal artery constriction. However, upward extension of the thrombus to involve a renal artery does occur in this disease and may produce severe hypertension. To our knowledge, the demonstration of this combination of circumstances has not been previously recorded. The present report deals with 3 such cases. In each, abdominal arteriograms were available before and after the development of hypertension and vividly portrayed the changes presumably responsible for the blood pressure elevation.