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Biomedical subjects

C E Atkins

Publications and source records attributed to C E Atkins.

46 records · Page 3Linked to original sources
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Systolic time intervals and their derivatives for evaluation of cardiac function.

Systolic time intervals provide a noninvasive indication of global left ventricular performance, are relatively sensitive, and are easily obtained from an M-mode echocardiogram. This paper defines systolic time intervals (preejection period, left ventricular ejection time, and total electromechanical systole) and their derivatives (preejection period/left ventricular ejection time and velocity of circumferential fiber shortening). Their utility and weaknesses, as well as the effects of heart rate, loading conditions, cardiac contractility, and drug therapies on systolic time intervals are discussed. Normal values for systolic time intervals for the dog and cat are provided.

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Intrapericardial cysts in the dog.

Intrapericardial cysts were identified as the cause of impaired cardiac filling in six young dogs. Pneumopericardiography and two-dimensional echocardiography showed the cysts in 2 of 2 dogs and in 4 of 4 dogs, respectively. One dog, which was also infected with heartworms, died before surgical excision of the cyst could be performed. In the remaining dogs, surgical excision of the cysts and subtotal pericardiectomy was successfully accomplished. Histologic examination of the excised tissue from one dog suggested that it was a pericardial coelomic cyst. The gross and histologic characteristics of the cysts removed from the other five dogs resembled those of acquired cystic hematomas. The etiopathogenesis of these cysts was uncertain, but all cysts were connected to a fatty pedicle of tissue. In one dog, a stalk of tissue was observed to enter the pericardium through a small peritoneopericardial diaphragmatic hernia. In four dogs, the stalk of tissue was adhered to the apex of the parietal pericardium. These observations suggested that intrapericardial cysts, in some dogs, develop in association with, and possibly as a result of, congenital herniation and entrapment of omentum or a portion of the falciform ligament into the pericardial sac.

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Orthodromic reciprocating tachycardia and heart failure in a dog with a concealed posteroseptal accessory pathway.

A 4-month-old male Labrador Retriever was presented for recurrent bouts of pulmonary edema associated with tachycardia. Initial physical examination and echocardiography were unremarkable, and the electrocardiogram revealed only an intraventricular conduction disturbance. Subsequent recordings showed paroxysmal supraventricular tachycardia (SVT) (340 beats/min), which consistently produced pulmonary edema. The supraventricular tachycardia was unresponsive to adenosine, esmolol, and propranolol; was variable and transiently responsive to various vagal maneuvers and precordial thumps; and was always responsive to IV diltiazem. Multiple life-threatening episodes of SVT occurred, however, despite the chronic administration of oral diltiazem, propranolol, and procainamide. Diastolic cardiac dysfunction was documented by Doppler echocardiography and was thought to contribute to the development of pulmonary edema. A subsequent electrophysiologic study confirmed the presence of an atrioventricular posteroseptal accessory pathway that participated in orthodromic reciprocating tachycardia. This pathway was determined to conduct only in the retrograde direction ("concealed accessory pathway"). Intraoperative IV procainamide titration terminated the arrhythmia, which could not be reinduced when procainamide blood concentration approximated 20 micrograms/dL. Increasing the oral procainamide dose to achieve such plasma concentrations was successful in eliminating orthodromic reciprocating tachycardia, preventing heart failure, and returning Doppler indices of diastolic function to normal.

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Pharmacokinetic and pharmacodynamic properties of conventional and CD-formulated diltiazem in cats.

The i.v. and apparent steady-state kinetics of diltiazem HCI (DLT) and slow-absorption long-acting diltiazem (CD) given p.o. were investigated in cats. The effects of p.o. diltiazem on heart rate and PR interval were also studied. Plasma diltiazem concentrations were determined by ultraviolet high-performance liquid chromatography (UV-HPLC), using verapamil as the internal standard. Heart rate and PR interval determinations were evaluated over a 24-hour period for the PO formulations and compared with values under diltiazemfree conditions. The mean systemic clearance and apparent volume of distribution of i.v. diltiazem were 15.0 mL/min/kg and 2.70 L/kg, respectively. The elimination half-life of diltiazem after i.v. and p.o. DLT administration were approximately 120 minutes. In contrast, the terminal half-life of CD was 460 minutes. The mean apparent bioavailability of DLT p.o. was 71%, which was significantly higher than that observed with CD (36%). Heart rate and PR intervals in cats receiving the 2 formulations at steady-state were not different from those measured in the drug-free state. We conclude that DLT at 1 mg/kg p.o. tid and CD at 10 mg/kg p.o. sid provide plasma concentrations that are known to have pharmacodynamic effects in other species.

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Systemic arterial dirofilariasis in five dogs.

Systemic arterial dirofilariasis is an unusual manifestation of heartworm disease of dogs that results from aberrant migration of Dirofilaria immitis into the peripheral arterial circulation. To expand the clinical characterization of systemic arterial dirofilariasis, 5 dogs evaluated at the North Carolina State University's College of Veterinary Medicine were reviewed. Common clinical presentations included hindlimb lameness, paresthesia of hindlimbs, and interdigital ischemic necrosis resulting from thromboembolic disease. Visualization of heartworms with angiography or ultrasonography confirmed the diagnosis in all cases. All 5 dogs were treated with an adulticide; 3 dogs were treated with thiacetasamide sodium and 2 with melarsomine dihydrochloride. Four of the 5 dogs survived the initial treatment period; 1 dog died of severe thromboembolic complications after thiacatarsamide sodium therapy. The treatment of systemic arterial dirofilariasis creates a therapeutic challenge because of multiple potential complications resulting from thromboembolic disease.

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Evaluation of the effect of pleural effusion on central venous pressure in cats.

This study was undertaken to determine if pleural effusion (PEF) increases central venous pressure (CVP) in cats, to define any relationship between volume of PEF and CVP and to ascertain the significance of CVP alterations in cats having PEF and suspected right heart failure (RHF). CVP was measured from a jugular vein before (CVPpre) and after (CVPpost) bilateral thoracentesis in 9 cats with naturally occurring PEF and under experimental conditions in 3 spontaneously breathing anesthetized cats receiving graded intrathoracic infusion of saline. Volumes of introduced and recovered fluid were recorded. A significant decrease occurred in CVP after thoracentesis in cats with naturally occurring PEF (mean difference, 4.5 cm H2O; range, 0-7.0 cm H2O, P < .005). The magnitude of change in CVP was constant (r = 0.36, P > .05) over the range of volumes recovered (range, 95-450 mL or 16.4-90 mL/kg). Five cats had CVPpre suggestive of RHF (range, 8.16-20.4 cm H2O). After thoracentesis, RHF was ruled out in 1 cat (CVPpost, 4.08 cm H2O) and the CVP declined but remained abnormally high (9.52 cm H2O) in 1 cat with a mediastinal mass. In 2 cats with confirmed RHF (CVPpre, 20.4 and 16.3 cm H2O), CVP decreased after thoracentesis but remained abnormally high (CVPpost, 14.96 and 10.88 cm H2O). In 1 cat with noncardiogenic PEF and inadequate removal of fluid, CVPpost (8.16 cm H2O) did not decrease. Experimentally, a positive linear relationship was observed between CVP and volume of PEF. The threshold volume required to increase CVP (17 mL/kg) approximated that suggested by clinical observation (22 mL/kg). PEF increases CVP and can cause abnormally high CVP in the absence of RHF.

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Natural history of hypertrophic cardiomyopathy and aortic thromboembolism in a family of domestic shorthair cats.

A feline domestic shorthair queen and her 3 offspring were all diagnosed with asymptomatic hypertrophic cardiomyopathy (HCM). The family has been followed for 13 years, and 3 cats have died of aortic thromboembolism (ATE). This communication documents the long-term progression of HCM in these cats that presented with mild left ventricular hypertrophy and hyperdynamic systolic ventricular function, developed progressive left atrial enlargement, and eventually resulted in hypodynamic left ventricular systolic function with relative left ventricular chamber dilation at the time of ATE.

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Percutaneous balloon pericardiotomy as a treatment for recurrent pericardial effusion in 6 dogs.

Percutaneous balloon pericardiotomy (PBP) has been performed in people and in a small number of dogs as a treatment for recurrent pericardial effusion with tamponade (PET). We performed this technique on 6 dogs with recurrent PET (5 with heart base tumors and 1 with no identifiable mass). Under general anesthesia and fluoroscopic guidance, a balloon-dilating catheter (diameters 14-20 mm) was introduced percutaneously at the 5th intercostal space through a sheath-introducing catheter, positioned across the parietal pericardium, and inflated 3 times. No dog experienced serious complications. The procedure was considered successful in 4 of 6 dogs. One dog is still alive without recurrence of PET 1 year after the procedure. Three dogs died of unrelated disease without recurrence of PET 5. 19, and 32 months after the procedure. The procedure was not beneficial in 1 dog that was euthanized 9 weeks later because of recurrence of pleural and abdominal effusion thought to be secondary to PET. One dog may have temporarily benefited but developed symptomatic PET 6 months after PBP. PBP appears to be a safe, economical, and potentially effective palliative treatment for recurrent PET and is a reasonable, less invasive alternative to surgery for dogs with recurrent PET, especially effusions caused by heart base tumors and possibly idiopathic pericardial effusion. Premature closure of the stoma is a potential cause for long-term failure and was thought to have been responsible for the recurrence of clinical signs in 2 dogs.

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Myocardial infarction complicating management of congestive heart failure in a dog.

A 7.5-kg, 10-year-old, spayed female, mixed-breed dog was evaluated for sudden onset of weakness, tachypnea, and an irregular cardiac rhythm. Congestive heart failure secondary to mitral valve regurgitation had been diagnosed six weeks earlier. The dog was stable on furosemide, enalapril, and hydralazine. Complex ventricular tachycardia, altered QRS conformation of sinus complexes, echocardiographic evidence of a hypokinetic left-ventricular free wall, and elevated creatine kinase suggested a diagnosis of myocardial infarction. Despite antiarrhythmic therapy, the dog developed ventricular fibrillation and died 36 hours after admission. Postmortem examination confirmed the myocardial infarction. Although a rare diagnosis in the veterinary patient, myocardial infarction must be considered in the differential diagnosis for sudden onset of weakness, tachypnea, and ventricular tachycardia.

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