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Оглавление

Cardiac Disease

BASICS

DEFINITION/OVERVIEW

Cardiovascular disease encompasses a group of disorders of the heart and blood vessels including:

Cardiomyopathy

Septic endocarditis

Valvular insufficiency (with no current evidence of primary degenerative endocardiosis)

Myocarditis

Pericardial effusion

Infarct

Atherosclerosis

Aneurysm (rupture of aortic or carotid aneurysm)

Gout

Arterial calcification

Thrombus

Parasitic infestations

Congenital heart defects

Tumors

ETIOLOGY/PATHOPHYSIOLOGY
Infectious

Often secondary to systemic infections in captive reptiles.

Bacterial: aerobic Gram‐negative bacteria: Salmonella spp., Corynebacterium spp., Pseudomonas spp. (endocarditis). Flavobacterium spp. and Vibrio spp. in a Barber’s map turtle (Graptemys barbouri) (myocarditis).

Parasitic: Trematodes (spirorchid flukes: Spirorchis spp., Learedius spp.) have been reported in the heart chambers and major vessels of sea and freshwater turtles (Chelonia mydas, Trachemys scripta elegans, Chrysemys picta), causing arteritis, endocarditis, granulomatous myocarditis, thrombosis and aneurysm.

Non‐Infectious

Neoplastic (primary neoplasia is uncommon in reptiles): hemangioma, hemangiosarcoma, cardiac rhabdomyosarcoma, fibrosarcoma; disseminated coelomic papillomas affecting various organs, including the heart, are frequently found in sea turtles with fibropapillomatosis.

Metastasis to the heart: metastatic chondrosarcoma, metastasis of oviductal adenocarcinoma, disseminated mast cell tumor, multicentric lymphoblastic lymphoma and lymphoblastic malignant lymphoma.

Metabolic: visceral gout can cause urate crystals deposition in the pericardium.

Cardiomyopathy is of undetermined origin in reptiles. Myocardial degeneration can be the consequence of gout (of metabolic, nutritional or iatrogenic origin) and/or vitamin E and selenium deficiencies. The myocardium and the major arteries may also be subject to mineralization (calcification) with a diet of excessive levels of calcium and vitamin D3.

Pericardial effusion is reported in many species but a small amount of fluid within the pericardial sac may also be normal. The etiology of pathologic pericardial effusion is unknown.

SIGNALMENT/HISTORY

There are no known species, sex, or age predilections.

Weakness and dyspnea

Swelling in the area of the neck and/or peripheral edema.

CLINICAL PRESENTATION

Presentation is similar to that seen in mammals.

Some differences exist due to differing cardiovascular physiology and anatomy.

Non‐specific clinical signs such as lethargy, depression, anorexia, weight loss, weakness, dyspnea, bilateral exophthalmia, and sudden death.

Cyanosis

Peripheral edema (e.g., in gular region)

Pulmonary edema, ascites

Neurological signs such as ataxia and head tilt in case of brain anoxia.

Peripheral thrombosis and necrosis in case of filarial infestation of the cardiovascular system.

Coughing is not a feature of congestive heart failure as observed in mammals.

RISK FACTORS

Husbandry

Inadequate husbandry, resulting in chronic stress, immune suppression and malnutrition, is the most likely common predisposing factor for the development of cardiovascular conditions in captive reptiles.

Others

Atherosclerosis and viral diseases can also be predisposing factors.

DIAGNOSIS

DIFFERENTIAL DIAGNOSIS

All other diseases that induce lethargy and/ or respiratory distress.

DIAGNOSTICS

Ambient temperature can influence cardiopulmonary parameters in reptiles so must be considered during examination.

Auscultation

The use of a stethoscope is impossible because of the osteodermic shell.

A continuous Doppler ultrasonic probe (8 MHz) can also be used for cardiac “auscultation”. It allows determination of heart rate and rhythm but only indicates blood flow (not valve closure).

Ultrasound

The most practical diagnostic tool for antemortem evaluation of reptilian heart diseases.

Allows visualization of blood flow within the heart. In chelonians, the transducer is placed in the cervicobrachial area.

Hematology and Biochemistry

Blood pressure measurement and pulse oximetry are not reliable in reptiles.

Clinical Pathology

CK and LDH may increase with conditions affecting the cardiac muscle in reptiles, such as myocarditis or infarct. However, these are non‐specific measurements and may also increase with skeletal muscle damage from traumatic injuries, loss of body condition, and intramuscular injections.

Currently, cardiac troponins have not been assessed in chelonians.

Leukocytosis, lymphocytosis, and heterophilia may be present, and are suggestive of underlying infections or hematopoietic neoplasia with secondary cardiac effects.

Electrocardiography

Low electric amplitudes (usually < 1.0 mV) and standard parameters not established for many species.

Common findings in the normal reptilian ECG include P‐wave pleomorphism, very small Q and S deflections and prolonged Q‐T intervals compared with similar‐ sized mammals.

Correct electrode placement (challenging in reptiles) is essential to avoid erroneous ECG readings.

Radiography

Challenging to produce images of high diagnostic value, especially in chelonians.

CT and MRI

Apart from obvious cardiomyopathy, neither CT nor MRI (unless using a very high magnetic field strengths) are of use for visualizing intracardiac structures and large vessels.

Evaluate for concurrent disease to determine whether cardiac issue is primary or secondary (neoplastic, infectious).

PATHOLOGICAL FINDINGS

Gross and histopathologic findings depend on the type of heart disease.

TREATMENT

APPROPRIATE HEALTH CARE

Little information

The pharmacology of cardiac drugs in reptiles is poorly understood and few data are available in the literature (pharmacokinetics, toxicity, etc.).

NUTRITIONAL SUPPORT

No specific nutritional support considerations or recommendations.

CLIENT EDUCATION/HUSBANDRY RECOMMENDATIONS

Reduce stress by minimizing handling, separating from cage mates, and maintaining the reptile at its preferred optimum temperature.

MEDICATIONS

DRUG(S) OF CHOICE

Beta‐blockers: of unknown effectiveness in reptile patients.

Methylatropine: administration results in an increase in resting heart rate of iguanas (Iguana iguana). No data available for chelonians.

Pimobendan and digoxin: unknown effects in reptiles.

Enalapril: inhibited angiotensin I conversion in alligators at 0.5–0.7 mg/kg once every 24 hours (combined with spironolactone and furosemide). No data available for chelonians.

Furosemide: possible diuretic effect in chelonians despite lacking the loop of Henle.

Hydrochlorothiazide has been used as a diuretic in lizards with renal disease. No data available for chelonians.

Methylated xanthines (aminophylline and theophylline) have successfully induced diuresis.

Nothing is known about the potential use of spironolactone in reptiles.

PRECAUTIONS/INTERACTIONS

N/A

FOLLOW‐UP

PATIENT MONITORING

Hemoculture, repeated echocardiographic examinations

EXPECTED COURSE AND PROGNOSIS

As no specific treatment is available, fast deterioration can be expected.

MISCELLANEOUS

COMMENTS

N/A

ZOONOTIC POTENTIAL

Can be zoonotic in case of salmonellosis and other Gram‐negative bacteria.

SYNONYMS

Cardiovascular disease

Heart disease

ABBREVIATIONS

CK = creatine kinase

CT = computed tomography

ECG = electrocardiogram

LDH = lactate dehydrogenase

MRI = magnetic resonance imaging