Hypertensive Heart Disease and Nutritional and Metabolic Disorders

Hypertensive, nutritional, and metabolic disorders have diverse presentations and adversely affect multiple organ systems. Heart disease is common, but it is often subclinical and detected only when noninvasive studies such as echocardiography are performed. Cardiovascular disease is a major source of morbidity and mortality in many metabolic disorders, and the ability to detect early cardiac changes is important. Early treatment of the underlying disorder can reverse the cardiac disease process ( Table 34.1 ). However, when left untreated, these disorders lead to myocardial fibrosis that results in permanent cardiac dysfunction and increased mortality rates.

TABLE 34.1

Cardiac-Relevant Clinical Guidelines and Scientific Statements for Management of Nutritional and Metabolic Disorders.

Year	Name	Organizations	Content
Hypertension
2015	Recommendation on the Use of Echocardiography in Adult Hypertension	European Association of Cardiovascular Imaging and American Society of Echocardiography		Echocardiography laboratory standards for adult hypertension
2017	Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults	American College of Cardiology and American Heart Association		Practice recommendation for measurement and management of hypertension
Obesity Related
2009	Clinical Guideline for the Evaluation, Management, and Long-Term Care of OSA in Adults	American Academy of Sleep Medicine		Screening and diagnostic strategies for OSA Treatment options for OSA
2011	Bariatric Surgery and Cardiovascular Risk Factors	American Heart Association		Types of bariatric surgery Complications of bariatric surgery Effect of bariatric surgery on CV risk factors and survival
2013	Management of Overweight and Obesity in Adults	American College of Cardiology American Heart Association The Obesity Society		BMI cut points to determine risk Impact of weight loss on risk Dietary intervention strategies Bariatric surgery effectiveness
2015	Cardiac Chamber Quantification by Echocardiography in Adults	American Society of Echocardiography European Association of Cardiovascular Imaging		Indexing for body size Chamber size and function measurements standards Normal ranges for echocardiographic parameters
Diabetes
2015	Update on Prevention of Cardiovascular Disease in Adults with T2DM	American Diabetes Association American Heart Association	New diagnostic criteria for T2DM Lifestyle management of T2DM Treatment targets in T2DM Screening for CV diseases in T2DM
2016	Contributory Risk and Management of Comorbidities of Hypertension, Obesity, Diabetes Mellitus, Hyperlipidemia, and Metabolic Syndrome in Chronic Heart Failure	American Heart Association	Management of comorbidities in patients with heart failure
Liver Disease
2012	Cardiac Disease Evaluation and Management Among Kidney and Liver Transplantation Candidates	American College of Cardiology American Heart Association	CAD evaluation and management of transplant candidates Evaluation for pHTN for liver transplant candidates Medical management of CV risk in transplant candidates
2013	Evaluation for Liver Transplantation in Adults	American Association for the Study of Liver Disease American Society of Transplantation	Indications for liver transplantation Cardiac evaluation for liver transplantation

BMI, Body mass index; CAD, coronary artery disease; CV, cardiovascular; OSA, obstructive sleep apnea; pHTN, pulmonary hypertension; T2DM, type 2 diabetes mellitus.

Hypertension

Background

Hypertension is the most prevalent modifiable risk factor for cardiovascular events. Almost one half of the US adult population has elevated blood pressure based on the 2017 US guidelines. Elevated systemic arterial blood pressure leads to maladaptive changes in left ventricular (LV) size, geometry, and function. Prolonged exposure increases the risk of clinical heart failure and cardiovascular death.

Echocardiography is the most common imaging modality for evaluating changes in myocardial structure and performance. The benefit of routine echocardiography for all hypertensive patients without symptoms or signs of hypertensive heart disease is uncertain, and it may be costly due to the widespread burden of disease. The decision to pursue echocardiography should be guided by how the results will change management. When patients have symptoms and signs that suggest hypertensive heart disease, an echocardiogram is appropriate.

Echocardiographic Findings

The most notable change in cardiac structure from systemic arterial hypertension is an increase in LV mass. LV mass is calculated from M-mode measurements of the interventricular septal wall (IVS), the LV diastolic internal dimension (LVID), and the posterior wall (PW) using this well-validated formula :

\begin{matrix} LV mass = [1.04 × {(LVID + IVS + PW)}^{3} - {LVID}^{3}] \\ × 0.8 + 0.6 \end{matrix}

$\begin{matrix} LV mass = [1.04 × {(LVID + IVS + PW)}^{3} - {LVID}^{3}] \\ × 0.8 + 0.6 \end{matrix}$

Modern image processing provides well-defined visualization of endocardial borders, allowing measurements to be made from the tissue-blood interface as opposed to the original leading edge–to–leading edge standard. When cardiac orientation does not allow M-mode measurements to be perpendicular to the LV long axis, two-dimensional (2D) echocardiography–guided linear measurements should be used. LV mass calculated from linear measurements is limited by several geometric assumptions about the three-dimensional (3D) heart. LV mass calculations subtract the ventricular cavity volume from the LV epicardial volume, and 2D and 3D techniques make fewer assumptions about the volume estimation ( Fig. 34.1 ). Although 3D techniques can overcome some limitations compared with the linear formula, 3D echocardiography relies more on image quality. The normal ranges for a 3D LV mass have not been as well validated as estimations made with the use of linear measurements. When making comparisons of changes between serial studies, measurements should be made with the same technique.

Fig. 34.1, 3D echocardiographic assessment of an LV mass.

LV hypertrophy (LVH) can be categorized as different geometric patterns based on the relative wall thickness (RWT), body surface area, and gender ( Table 34.2 and Fig. 34.2 ). RWT is calculated as 2 × PW/LVID or (PW + IVS)/LVID, but the latter is less accurate in the setting of a significant basal septal bulge. The most common remodeling pattern from hypertension is concentric hypertrophy. Geometric classifications can provide additional prognostic information beyond LV mass. Refinement in classification using LV volumes provides additional prognostic information. An increased LV mass-to-volume ratio has been associated with high rates of fibrosis, myocardial dysfunction, and adverse cardiovascular outcomes.

TABLE 34.2

Left Ventricular Geometric Patterns.

Geometry	Mass	Regional Wall Thickness
Normal	≤115 g/m ² (men) ≤95 g/m ² (women)	≤0.42
Concentric hypertrophy	>115 g/m ² (men) >95 g/m ² (women)	>0.42
Eccentric hypertrophy	>115 g/m ² (men) >95 g/m ² (women)	≤0.42
Concentric remodeling	≤115 g/m ² (men) ≤95 g/m ² (women)	>0.42

Fig. 34.2, Geometric patterns of LV hypertrophy.

LV function is adversely affected by hypertension and cardiac remodeling. Systolic function is most commonly assessed using EF, but in concentric hypertrophy, the EF is less accurate for systolic performance (see Chapter 4 ). A high systemic afterload impairs cardiac emptying, leading to a lower EF measurement without a change in myocardial contractility. Conversely, concentric hypertrophy with wall thickening increases the EF for any given level of contractility. When technically feasible, alternative measures can be made such as midwall fractional shortening or LV global longitudinal strain ( Fig. 34.3 ). Diastolic dysfunction more commonly occurs before changes in systolic function in hypertensive patients. Diastolic evaluation to include mitral inflow measurements, mitral annular tissue Doppler, and LA size should be performed in all studies (see Chapter 5 ).

Fig. 34.3, Measurements of systolic function in a hypertensive patient.

Clinical Interventions

The decision to begin antihypertensive therapy is based on clinical parameters, including cardiovascular risk and blood pressure measurements. Studies have shown that intensive blood pressure goals for people at elevated cardiovascular risk reduce cardiovascular events. Although treatment recommendations for antihypertensive therapy may be affected in individuals with a reduced ejection fraction (EF), they otherwise do not depend on the more common hypertensive findings of LVH, diastolic dysfunction, or abnormal cardiac remodeling.

Blood pressure lowering can lead to a reduction in LV mass. Initial recommended therapies with thiazide diuretics, calcium channel blockers, angiotensin-converting enzyme inhibitors, and angiotensin receptor blockers have demonstrated higher rates of LVH regression compared with β-blocker therapies. However, observational registries have shown that LV regression is not as commonly observed in the general population as in clinical trials and may not have a large impact on clinical outcome. ^, This finding may in part result from LVH and diastolic dysfunction not being specific to hypertension, but there also may be an association with other common comorbidities such as obesity, obstructive sleep apnea, and diabetes. In a subanalysis from Anglo-Scandinavian Cardiac Outcomes, LV regression failed to correlate with improvement in diastolic parameters. Echocardiography for evaluation of antihypertensive treatment effects on cardiac structure is not recommended.

Obesity

Background

Obesity is a chronic disease of excessive body fat. It is a worldwide epidemic with increasing global prevalence over the past 3 decades. In developed countries, most men are clinically categorized as overweight or obese. Obesity has serious impact on overall health, with an increasing risk of cardiovascular comorbidities and a 40% increased risk of vascular mortality. Medical providers commonly order echocardiographic evaluations for obese individuals with concerning symptoms (e.g., dyspnea on exertion) that may be related to underlying cardiac dysfunction or decreased cardiorespiratory fitness.

There are several measures of adiposity using anthropometric measurements or noninvasive imaging to directly measure visceral fat content; however, the most practical and recommended assessment of obesity remains the body mass index (BMI). The BMI can be easily calculated by dividing body weight in kilograms by height in meters squared (kg/m ² ). BMI categories accurately stratify all-cause and cardiovascular mortality risks ( Table 34.3 ).

TABLE 34.3

All-Cause and Ischemic Heart Disease Adjusted Mortality Rates Stratified by Body Mass Index Classification.

WHO Category	BMI (kg/m ² )	All-Cause Mortality Rate (Men) ^a	All-Cause Mortality Rate (Women) ^a	IHD Mortality Rate ^a
Underweight	<18.5	18.4	10.5	2.6
Normal weight	18.5–24.9	14.5	8.9	2.7
Overweight	25–29.9	16.9	10.4	3.5
Obesity class I	30–34.9	22.7	13.0	5.8
Obesity class II	35–39.9	28.2	17.0	7.8
Obesity class III (severe)	≥40	34.7	19.2	8.3

BMI, Body mass index; IHD, ischemic heart disease; WHO, World Health Organization.

a Adjusted annual rates of cases per 1000 patients as calculated by Whitlock et al.

BMI is a whole-body measure, and it may overestimate or underestimate adiposity in highly muscular individuals and Asian populations, respectively. Additional measures of abdominal obesity such as waist circumference and body fat percentage may provide complementary information in these situations. Computed tomography (CT) and magnetic resonance imaging (MRI) can determine visceral fat distribution and mass but remain too expensive for clinical use.

Direct pathophysiologic consequences of obesity on cardiac structure and function include hemodynamic, neurohormonal, and metabolic alterations. Increased fat mass is associated with increased blood volume, cardiac output, and LV stroke work. A larger venous return increases LV filling pressures and wall stress, leading to cardiac remodeling with varied responses in LV geometry depending on the duration of obesity and comorbidities.

Animal and human studies have shown obesity-associated inflammatory responses from hypertrophied adipocytes. Epicardial fat deposits produce localized hypoxia leading to dysregulated adipocyte secretion of proinflammatory cytokines. The increased triglyceride content and fatty acid use in cardiomyocytes with obesity can lead to myocardial dysfunction. These mechanisms are likely responsible for the development of an obesity cardiomyopathy and a doubling in the incidence of clinical heart failure.

Echocardiographic Findings

Technical Considerations

Ultrasound image quality is adversely affected by obesity. Ultrasound energy is attenuated by excessive chest wall fat tissue and by the increased depth of insonation from large chest walls. Lower transducer frequencies, nontraditional views, proper patient positioning, and echocardiographic contrast can be used to improve image quality. Although echocardiographic image quality may be degraded more than in CT or MRI studies, these techniques may not be technically feasible for patients with severe obesity due to the weight and size limits of imaging tables. For patients undergoing bariatric surgery, technically difficult stress echocardiography is associated with worsening levels of obesity, but adequate studies can be almost universally achieved in experienced centers using contrast agents.

Another important technical consideration is scaling of cardiac measurements for body size with obesity. The American Society of Echocardiography Chamber Quantification Guidelines recommend ratio-metric (linear) indexing of LV size and mass to body surface area (BSA). Indexing measurements may allow normalization of parameters to refine the assessment of pathologic versus physiologic changes; however, in severe obesity, BSA may not adequately normalize measurements. Alternative indexing of LV mass with fat-free measurements such as height can better predict adverse events in obese populations. Allometric (exponential) scaling of LV measurements produces more accurate correction in obesity. Similarly, indexing aortic valve area by BSA in obesity increases discordance between indexed and nonindexed valve area meeting criteria for severe aortic stenosis.

Structural Changes

Several changes in cardiac chamber sizes and geometry have been reported in obesity over the past 30 years. A significant association between obesity and LVH exists in almost all studies. The prevalence of LVH varies between 13% and 75% due to population characteristics of the study participants and the existence of common obesity-related comorbidities, such as hypertension or sleep apnea ( Fig. 34.4 ).

Fig. 34.4, Effect of the interaction of hypertension with obesity and nocturnal hypoxia on LV mass index.

Eccentric and concentric LVH patterns may be seen in obesity. Eccentric hypertrophy is associated with obesity measures because of the increased cardiac output and venous return. However, increased wall thickness with concentric remodeling and hypertrophy are common and may be more likely in older patients with coexisting hypertension. Obese adolescents without comorbidities or significant obesity duration present with thicker LV walls and larger LV masses compared with age-matched, normal-weight teenagers, indicating there are direct consequences of obesity on LV remodeling.

Diastolic Function

Diastolic function is commonly impaired in obese patients, and along with deconditioning, this leads to symptoms of dyspnea. Diastolic impairments have been demonstrated in relaxation and compliance of the LV; however, a grade I (i.e., impaired relaxation) mitral inflow filling pattern is most common. Tissue Doppler of the mitral annulus ( e ′) as a load-independent measure of relaxation is reduced in obesity. Invasive hemodynamic studies reveal higher LV filling pressures in severe obesity. An echocardiographic correlate of elevated filling pressures (E/ e ′) is also associated with higher BMI.

Although diastolic impairments are commonly related to LV structural changes in obesity, some studies have shown altered diastolic parameters with increasing BMI independent of LV mass and comorbidities. Alterations in diastology are seen in all age groups, from obese children to obese elderly individuals, compared with their age-matched controls, but the changes are usually only mild, and the severity does not appear to change with duration of obesity.

Systolic Function

Systolic function is typically assessed by LVEF measurements. Despite obesity-related structural and hemodynamic changes, there is no solid evidence that severe obesity by itself causes a clinically significant reduced EF. Alternative pathologies should be sought in obese individuals with dilated cardiomyopathies. Similar to hypertension-related LVH, obesity leads to increased endocardial shortening, preserving the EF, but midwall fractional shortening is modestly decreased.

Tissue Doppler and speckle tracking strain imaging provide load-independent measures of global and regional contractility. Reductions in systolic strain have been found with increasing BMI ( Fig. 34.5 ). Speckle tracking strain measurements, although promising, require high-quality 2D images, which can be difficult to obtain in obese patients and require further standardization between vendors before they will be acceptable for routine clinical practice.

Fig. 34.5, Association of body mass index with longitudinal LV end-systolic strain.

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