Clinical Approach to Small Animal Cardiovascular Diseases

PRESENTATION

BROCHURE

CLINICAL APPROACH TO SMALL ANIMAL

Cardiovascular Diseases Claudio Bussadori

CLINICAL APPROACH TO SMALL ANIMAL

Clinical Approach to Small Animal Cardiovascular eBook available Diseases

Cardiovascular Diseases Claudio Bussadori

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This book combines basic science with clinical matter to provide readers with knowledge on the therapeutic management of canine and feline cardiovascular diseases, based on their pathogenic and pathophysiological mechanisms. The chapters include histopathological, anatomopathological, imaging, and clinical figures, as well as online videos to illustrate diagnostic and therapeutic procedures.

TARGET AUDIENCE:

✱ Small animal vets. General practice, cardiology, internal medicine ESTIMATED FORMAT: 21.6 × 28 cm RETAIL PRICE NUMBER OF PAGES: 432 approx.

NUMBER OF IMAGES: 350 approx.

BINDING: hardcover ISBN: 978-88-214-4940-6 ESTIMATED PUBLISHING DATE: January 2021

€89

Author CLAUDIO BUSSADORI DVM, MD, PhD, Dip. ECVIM-CA (cardiology).

Director and cardiology consultant at Gran Sasso Veterinary Clinic, Italy. Researcher in the Department of Paediatric Cardiology at San Donato Hospital, Italy.

COLLABORATORS M.ª Josefa Fernández del Palacio Jens Häggström Massimiliano Tursi Michele Borgarelli

KEY FEATURES:

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Step-by-step logical and systematic approach Clinically applicable information for veterinary professionals Over 350 photos and illustrations Videos to help illustrate diagnostic and therapeutic procedures

Clinical Approach to Small Animal Cardiovascular Diseases

Presentation of the book The aim of this work is to provide the reader with knowledge about the therapeutic management of canine and feline cardiovascular diseases based on an understanding of the pathogenic and pathophysiological mechanisms behind them.

Due to the fact that basic sciences and clinical topics are usually proposed separately in books, readers tend to ignore introductory subjects and learn clinical subjects using mnemonics. Conversely, this book effectively combines basic science with clinical matter.

Cardiovascular anatomy and physiology are described with practical references to the pathologies discussed in the clinical part; for instance, in the chapter about cardiovascular anatomy, the figures are composed not only of illustrations and photographs of anatomical findings but also of images from ultrasonography and radiography as well as from more advanced imaging technologies such as selective angiography and computed tomography that will illustrate the characteristics of species and breed. In turn, the section on cardiovascular embryology is aimed at introducing the teratogenic mechanisms that lead to the genesis of congenital heart disease.

The instructional videos included throughout the book illustrate the diagnostic and therapeutic procedures that can be better appreciated with moving images.

hkeita/shutterstock.com

Likewise, in the chapters about the different diseases, the understanding of their pathogenic mechanisms is deepened through an accurate description of the pathophysiology and the use of numerous images and references of histopathology and pathological anatomy. This will allow to assess disease severity, which is useful for staging, therapeutic choice, and counselling for breed screening.

The author Claudio Bussadori Dr Bussadori obtained his degree in veterinary medicine in 1982. He became a founding diplomate of the European College of Veterinary Internal Medicine (ECVIM) - Companion Animals, subspecialty cardiology, in 1993. He was vice president of the ECVIM between 1993 and 1999 and president of the European Society of Veterinary Cardiology (ESVC) between 1997 and 1999. Dr Bussadori graduated in medicine in 2001 and has been an honorary member of the ESVC board since 2002. He obtained his PhD in cardiovascular physiology in 2007.

Dr Bussadori combines his work as director, cardiology consultant, and director of an ECVIM residency programme on cardiology at Gran Sasso Veterinary Clinic with his research activity in the Department of Paediatric Cardiology at San Donato Hospital in Milan, Italy. His research focuses on echocardiography and interventional treatment of congenital heart diseases in dogs and humans. Dr Bussadori has authored more than 160 publications including book chapters, research articles published in medical and veterinary journals, and congress abstracts.

Clinical Approach to Small Animal Cardiovascular Diseases

Collaborators M.ª Josefa Fernández del Palacio Dr Fernández obtained a degree and a PhD in veterinary medicine. Diplomate of the European College of Veterinary Internal Medicine - Companion Animals, subspecialty cardiology, she is a professor at the University of Murcia, Spain.

Jens Häggström Dr Häggström obtained a degree and a PhD in veterinary medicine. Diplomate of the European College of Veterinary Internal Medicine - Companion Animals, subspecialty cardiology, he is a professor at the University Animal Hospital (UDS) of the Swedish University of Agricultural Sciences, Sweden.

Massimiliano Tursi Dr Tursi obtained a degree and a PhD in veterinary medicine. Member of the Italian Association of Veterinary Pathologists and the European Society of Veterinary Pathology, he is an assistant professor of pathology in the Department of Animal Pathology at the University of Turin, Italy.

Dr Borgarelli obtained a degree and a PhD in veterinary medicine. Diplomate of the European College of Veterinary Internal Medicine - Companion Animals, subspecialty cardiology, he is an associate professor at the Virginia–Maryland College of Veterinary Medicine, United States.

hkeita/shutterstock.com

Michele Borgarelli

Table of contents 1. Cardiovascular anatomy 2. Cardiovascular physiology 3. Introduction to congenital heart disease 4. Congenital heart disease with increased pulmonary blood flow 5. Congenital heart disease with decreased pulmonary blood flow 6. Congenital heart disease with obstruction to blood progression and no septal defect 7. Vascular ring anomalies and other vascular anomalies 8. Uncommon types of congenital heart disease 9. Myxomatous valvular heart disease 10. Degenerative valvular disease 11. Infective endocarditis 12. Canine cardiomyopathy 13. Feline cardiomyopathy 14. Pericardial disease 15. Cardiac tumors 16. Pulmonary hypertension 17. Cardiovascular effects of systemic diseases and metabolic disorders

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CLINICAL APPROACH TO SMALL ANIMAL

Cardiovascular Diseases Claudio Bussadori

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CHAPTER

16

Pulmonary hypertension Claudio Bussadori

INTRODUCTION Pulmonary hypertension (PH) is a pathological haemodynamic condition defined as an increase in systolic and mean pulmonary arterial pressure (PAP) respectively, higher than 30 and 25 mmHg. In the earliest stage of PH, the PAP may be normal at rest, but increases severely during exercise. Subsequently, in more advanced stages, it is also increased at rest. Chronic elevation of PAP and pulmonary vascular resistance (PVR) lead to right ventricular enlargement and hypertrophy. When the adaptative mechanisms of right ventricular dilation and hypertrophy become inadequate to the afterload, right sided heart failure occurs, condition associated with poor prognosis.

The severity of the symptoms and prognosis of pulmonary hypertension, the responsiveness to therapy and therefore the reversibility of the process, other than the pressure value found, depend on the cause of hypertension itself, on the rapidity of the progression of lesions in the pulmonary circulation, and the age of patient at which these occur, and the anatomical and functional remodeling of the right ventricle. A more precise definition of the haemodynamic profile of the patient can be performed with a cardiac catheterization, therefore with a direct measurement of pressures, the flow rate in the pulmonary circulation and the PVR. In veterinary clinical practice, cardiac catheterization should be performed only in some specific cases in which the aetiology is not clear or for some patients with congenital heart disease where accurate determination of pulmonary resistance is essential to establish the feasibility of a corrective intervention.

For almost all cases of pulmonary hypertension, echocardiography provides all the information needed for staging the disease, identifying the type of pulmonary hypertension and follow-up, avoiding the invasiveness, the cost and the procedural risk of cardiac catheterization.

The prognosis of pulmonary hypertension depends mainly on: â– Rapidity of progression of vascular remodeling. â– Reversibility of the vascular lesion.

Age of the patient at the time of the onset of the pulmonary hypertension.

EPIDEMIOLOGY AND AETIOLOGY OF PULMONARY HYPERTENSION Pulmonary hypertension is a relatively infrequent disease almost always diagnosed in dogs; it is very rarely found in cats. Unfortunately, there are no multicenter epidemiological studies but only published data on relatively small populations with diagnoses performed in individual centers.

Almost all these studies agree in identifying pulmonary hypertension due to left heart failure as the most frequently diagnosed form in dogs.

On a series of 26,000 cases referred for cardiology consultation to the Gran Sasso Veterinary Clinic (CVGS) in Milan from 1997 to 2019, the incidence of pulmonary hypertension was 276 cases, therefore 1% of cases reported with a prevalence of 13 cases per year.

According to studies published in the majority of patients with pulmonary hypertension, 51% of cases have been recognized to be caused by left heart failure; the other most frequently recognized causes are chronic pulmonary thromboembolism and idiopathic pulmonary hypertension. In this respect, in humans, a familiarity that in dogs is only suspected on the basis of anecdotal case histories has also been recognized (Table 27.1). The incidence of pulmonary hypertension caused by parasitic 1

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Acquired cardiovascular diseases

FIGURE 27.1. Small artery with severe mid-intimal hyperplasia with fibrosis and consequent lumen occlusion. 20×, Masson’s Trichrome.

FIGURE 27.2. Large artery with severe plexiform lesion. 5×, Weigert Van Gieson.

CARDIAC REMODELLING In physiological conditions, the right ventricle’s systolic function is expressed predominantly in a longitudinal direction; the major contribution to it is given by the longitudinal fibers of the inner layer that start from the annulus of the tricuspid valve extending in the right outflow tract up to the pulmonary annulus. In addition to these longitudinal fibers, the systolic function of the right ventricle is also supported by the aberrant fibers of the outer layer which from

the left ventricle ending on the pulmonary annulus, and a thin middle layer of circumferential fibers that in physiological conditions provide only a minimal contribution to contraction.

Systolic contraction of the right ventricle begins in the inflow tract that, together with interventricular septum give the major contribution to the ejection of the stroke volume and then few milliseconds after goes ahead in the right ventricular outflow tract (RVOT). This temporal lag gives the

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Pulmonary hypertension

FIGURE 27. 6. Male WHWT, 12 years old. Right lateral (a) and ventro-dorsal view (b). The lung parenchyma appears diffusely radiopaque, the dilation of the right ventricle is highlighted by the increased contact between the outer surface of the outflow tract and the sternum in the lateral view and the reversed D shape morphology in the ventrodorsal view. The dilation of the pulmonary artery is recognized by the bulging of the cardiac silhouette between hours 12 and 3 and in the lateral view by the dorsal displacement of the trachea.

a

b

FIGURE 27.7. Male WHWT, 12 years old. Transverse CT scan, Bone Filter and Lung Window. Moderate increase of unstructured interstitial pattern, characterized by accentuation of pleural fissures, peribronchial cuffs and tiny peripheral emphysematous areas.

FIGURE 27.8. Male English Bulldog, 6 years old, with mild Type 3 PAH due to BAOS MMode of the left ventricle. During inspiration the RV diameter increases, the LV diameter decreases and the interventricular septum is flattened and displaced towards the left side.

In type 3 pulmonary hypertension, medical or surgical treatment should be directed to the underlying disease, while specific vasodilatory therapies specifically aimed at reducing PVR are counterindicated, because the use of pulmonary vasodilator drugs counteracts the vasoconstrictive phenomenon due to local hypoxia that diverts blood from areas of dysfunctional lung parenchyma to healthy ones, thus reducing respiratory exchanges and worsening the patient’s hypoxia. Meanwhile, if the therapy aimed at the treatment of specific pathology works, the pulmonary hypertensive state also regresses.

TYPE 4 PULMONARY HYPERTENSION DUE TO THROMBOTIC AND/OR EMBOLIC DISEASE This form of PAH is caused by pulmonary embolism, which causes the increase of PVR by occluding part of the pulmonary arteries. The causes of the formation of thrombi that embolize in the pulmonary circulation may be different; more frequently we recognize protein-losing gastrointestinal or renal diseases that reduce the plasma level of antithrombin 3 and predispose to the formation of thrombi, or other alterations of coagulation process and blood viscosity such as diffuse 11

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Acquired cardiovascular diseases

A a

B b

FIGURE 27.17. Two examples of systolic septal paradoxical motion due to Type 1 PAH in reversed PDA. (a) On the left, severe systolic septal paradoxical motion, reduced RV systolic function and cardiac output. (b) On the right, mild systolic septal paradoxical motion, conserved RV systolic function and conserved cardiac output.

FIGURE 27.18. Severe RV dilatation and systolic septal displacement toward the right ventricle in PAH due to acute pulmonary embolism with low cardiac output and acute uncoupling between RV afterload and systolic function.

In both mono and bidimensional views it is possible to observe the signs of the right-pressure overload with the systolic paradoxical motion of the interventricular septum. On these views, the flattening of the interventricular septum, the increased dimension of the right ventricular cavity and the reduction of the size of the left ventricular chamber give the figure of the ventricular interdependence and definitively of the reduction of systemic cardiac output (Fig. 27.17). In pulmonary hypertension the magnitude of systolic septal paradoxical motion is directly proportional to

VIDEO 27.1. Bubble study of a suspected reversed PDA.

PVR and inversely proportional to LV filling volume. Therefore, it is much more evident in type 1 and type 4 and is extremely evident in acute pulmonary thromboembolism, in which the afterload is suddenly increased, while the systolic function of the right ventricle and the left filling volume are severely reduced (Fig. 27.18), whereas in post-capillary type 2 PH will be much less evident, and will increase with the involvement of the precapillary component.

In type 3, the increase in PAP is always mild; however, the paradoxical movement assumes peculiar characteristics in brachycephalic patients with obstructive syndrome of the upper airways. During inhalation the increase in endothoracic pressure increases pulmonary pressure and the paradoxical movement of the septum is accentuated (Fig. 27.8).

Other specific features that may help the diagnosis is the identification of heartworms in the main pulmonary artery

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Pulmonary hypertension

and its proximal branches. In acute pulmonary embolism it is frequent to identify large thrombi in the pulmonary arteries or less frequently in the right cardiac cavities. These masses require to be differentiated from some cardiac tumours.

Thrombi have a regular homogeneous echotexture and may be floating in the cavity or attached only in the areas were the velocity of the blood flow velocity it is low such as in the right auricle. In some cases, 3D echocardiography is helpful do define the consistence and the extension of the contiguity with the cardiac structure (Fig. 27.19).

The right ventricular systolic function can be measured with traditional echocardiographic parameters such as FAC (Fractional Area Change) and TAPSE (Tricuspid Annulus Peak Systolic Excursion) or using more advanced technologies such as Tissue Doppler, Strain and Strain Rate 2D based.

FAC is an indirect parameter that measures the variation of the area of the inflow tract of the right ventricle with the same principle, so substantially with the same formula of the ejection fraction measured on the left ventricle. The major limitation compared to EF is that because of the complex anatomical structure of the RV with this measure we only quantify the change of dimension of the right ventricular inflow and do not take in account the outflow tract. TAPSE measures the longitudinal systolic displacement of the tricuspid annulus and normal values are influenced by the dimensions of the animals (Fig. 27.20). S’ wave of the tissue Doppler measured at tricuspid annulus measures the velocity of this systolic displacement a

and the longitudinal strain measures global and segmental systolic contraction of the lateral wall of the inflow of the right ventricle. All these parameters do not measure the global function of the right ventricle but simply the longitudinal function of the lateral wall. This, in normal conditions and in many diseases, is the major component of the RV function but in condition of severe hypertrophy and particularly in Eisenmenger’s syndrome the systolic function is expressed mostly transversally and for this reason these parameters must be interpreted with caution. Since all these parameters measure longitudinal function, when this is depressed all parameters must be concordantly decreased, but the influence of preload are not the same for any of these. FAC, TAPSE and longitudinal strain are strongly load dependent, with an increase in values as a function of an increase in preload, while their decrease will express the decrease in the functional reserve in response to the increase in afterload. In PAH this is not a real concern since it is very rare for PAH to be associated with a right ventricular volume overload that can counteract the reduction of TAPSE, FAC, S’ (Fig. 27.21) and longitudinal systolic strain which are the expression of the degree of reduction of the longitudinal systolic function (Fig. 27.22).

Between these parameters only the Strain rate and the acceleration of the isovolumetric contraction registered to the tissue Doppler are completely independent of the preload, the latter two parameters are closely correlated with the intrinsic contractility of the ventricular myocardium, however if in clinical practice the Strain Rate is applicable in b

FIGURE 27.19. (a) On the left: bidimensional right parasternal off-axis view of the right atrial cavity RA (right atrium); Cau VC (caudal vena cava); Cr VC (cranial vena cava). The shape and the echotexture suggest the thrombotic nature of the mass; Thr (thrombus). (b) On the right: threedimensional section of the right base of the heart from apical left parasternal, the thrombus protrudes into the right atrial cavity from the right auricle where it is attached.

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Acquired cardiovascular diseases

a

b

FIGURE 27.20. (a) On the left: reduced TAPSE value in a six-year-old female Maltese with Type 1 PAH due to Eisenmenger’s syndrome. (b) On the right: increased TAPSE in condition of right ventricular volume overload.

a

b

C

FIGURE 27.21. Three evolutive stages of systolic function in patients with severe Type 1 PAH. (a) On the left: conserved isovolumic acceleration time wave and little reduction of peak S wave which expresses mild reduction of the longitudinal systolic function. (b) In the middle: conserved IVA wave and reduced S’ wave, reduction of the longitudinal systolic function, in this case the transversal function was maintaining an adequate CO at rest. (c) On the right: end stage of systolic disfunction and the E’ wave express an increase in end diastolic pressure in the dilated right ventricle.

a

b

FIGURE 27.22. Longitudinal strain of the right ventricle. (a) On the left: conserved longitudinal systolic function (L. Strain = –30.9%). (b) On the right: reduced systolic function (L. Strain = –20%).

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