**2. Extrinsic cardiomyopathy**

Cardiomyopathies are a group of diseases of the myocardium reflecting mechanical and/or electrical dysfunction of the heart [1], and can be delineated as being either intrinsic or extrinsic. Intrinsic cardiomyopathies are those which originate in the heart muscle cells, and includes both conditions which typically influence the cardiac muscle cells alone (primary cardiomy‐ opathy) and systemic disorders which affect other tissues in the body in addition to cardiac muscle tissue (secondary cardiomyopathy). Primary cardiomyopathies are commonly genetic or acquired (e.g. inflammatory, physical stress, or physiologic stress induced). Secondary

© 2013 McLeod and Pierce; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2013 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

cardiomyopathies span a broad spectrum of etiologies including inflammation, toxicity, infiltrative, endocrine, nutritional, autoimmune, electrolyte imbalance, and neuromuscular.

vival rates are higher than for men, women with heart failure have a far worse quality of life [5]. The crucial link between maintaining adequate fluid return, and therefore cardiac out‐ put, and heart failure is reflected in the ability of resting heart rate to strongly and inde‐ pendently predict coronary events in women [6]. In a recent study of over 100,000 postmenopausal women, resting heart rate was found to predict myocardial infarction or coronary death with a risk ration of 1.6 (95% confidence interval of 1.49-1.89) when compar‐

Cardiomyopathy in Women: Second Heart Failure

http://dx.doi.org/10.5772/55433

267

**3. Anatomic and physiologic influences on venous and lymphatic return**

When ventricular function is preserved, the critical factor regulating CO is end-diastolic volume, which, through the Frank-Starling mechanism provides a non-neural, non-humorally mediated, regulation of stroke volume. End-diastolic volume is a function of venous and lymphatic return to the heart, which correspondingly, are dependent on circulatory system volume and venous/lymphatic system pressure. The importance of lymphatic return is not widely appreciated in the context of maintenance of circulatory volume, and venous pressure is often considered only in the context of high venous pressure being an indicator of heart failure. However, to fully understand extrinsic heart failure it is necessary to consider the

In supine posture, fluid pressures in the arterial system are approximately 100 mmHg, and pressures in the venous system range from 15-20 mmHg in the smallest vessels to approxi‐ mately 5 mmHg at the right atrium. The driving pressure to return venous blood back to the heart is therefore only 10-15 mmHg, or approximately 13-20 cm of water. Nonetheless, in the supine position this pressure is typically adequate to return venous blood from the lowest part of the body (typically the buttocks) back to the heart. In the upright position, however, hydrostatic forces (i.e. gravitational forces operating on the venous fluid column) add signif‐ icantly to arterial, venous, and capillary pressures. At the right atrium, fluid pressure drops to zero. Above the atrium, venous pressures become negative, venous blood readily flows back to the heart and the veins collapse. At the same time, hydrostatic forces serve to reduce arterial pressures by 40mmHg at the top of the head, and if this reduces arterial pressure below 60

Below the heart, venous pressure increases progressively with distance below the heart such that at the level of the feet venous pressure can exceed 100 mmHg; yet the driving return pressure (i.e. capillary pressure) remains at approximately 20 mmHg. Moreover, blood return to the heart must take place through the highly distensible venous system so that the volume of the venous system has the potential to increase significantly in upright posture. Hydrostatic effects also increase pressures in the arterial system below the heart, though the thick walled structure of arteries prevents significant dilation. However, the increased pressures in the capillaries result in increased extravasation, resulting in significant pooling of interstitial fluid

until interstitial fluid pressures increase to match capillary pressures (Figure 2) [8].

ing the highest (>76 bpm) to the lowest (<62 bpm) quintiles of resting heart rate.

profound influence of upright posture on venous and lymphatic return.

mmHg, regulation of cerebral perfusion can be significantly affected [7].

In contrast, extrinsic cardiomyopathies arise due to conditions which do not directly produce heart muscle cell abnormalities. These include the well known conditions of ischemia, hypertension, diabetes, and alcohol abuse, but also the less commonly considered condition of insufficient venous return. Insufficient venous return results in inadequate atrial filling and a correspondingly decreased CO. Decreased CO initiates a range of compensatory responses which eventually lead to progressive heart failure. Lower limb edema, as well as ascites development, are eblematic of inadequate fluid return to the right atrium, and fatigue is common as the heart cannot maintain sufficient CO to meet the body's metabolic needs. Nausea and loss of appetite arise as blood is shifted from the gastrointestinal tract to the vital organs, and palpitations occur as the heart adapts to reduced stroke volume by increasing the heart rate [2]. This latter compensatory mechanism induces cardiac stress and systolic hypertension, eventually leading to cardiomyopathy.

**Figure 1.** Left ventricular ejection fraction in men and women with congestive heart failure. *After Vasan, et al.1999*.

Heart failure arising from inadequate fluid return to the heart is most commonly experi‐ enced by women. It is well recognized that while half of heart failure patients are women [3], the characteristics of heart failure in women differ substantially from those observed in men. Specifically, heart failure develops later in life in women, is commonly associated with preserved systolic function (Figure 1) [4], less commonly involves ischemia, and, while sur‐ vival rates are higher than for men, women with heart failure have a far worse quality of life [5]. The crucial link between maintaining adequate fluid return, and therefore cardiac out‐ put, and heart failure is reflected in the ability of resting heart rate to strongly and inde‐ pendently predict coronary events in women [6]. In a recent study of over 100,000 postmenopausal women, resting heart rate was found to predict myocardial infarction or coronary death with a risk ration of 1.6 (95% confidence interval of 1.49-1.89) when compar‐ ing the highest (>76 bpm) to the lowest (<62 bpm) quintiles of resting heart rate.

cardiomyopathies span a broad spectrum of etiologies including inflammation, toxicity, infiltrative, endocrine, nutritional, autoimmune, electrolyte imbalance, and neuromuscular. In contrast, extrinsic cardiomyopathies arise due to conditions which do not directly produce heart muscle cell abnormalities. These include the well known conditions of ischemia, hypertension, diabetes, and alcohol abuse, but also the less commonly considered condition of insufficient venous return. Insufficient venous return results in inadequate atrial filling and a correspondingly decreased CO. Decreased CO initiates a range of compensatory responses which eventually lead to progressive heart failure. Lower limb edema, as well as ascites development, are eblematic of inadequate fluid return to the right atrium, and fatigue is common as the heart cannot maintain sufficient CO to meet the body's metabolic needs. Nausea and loss of appetite arise as blood is shifted from the gastrointestinal tract to the vital organs, and palpitations occur as the heart adapts to reduced stroke volume by increasing the heart rate [2]. This latter compensatory mechanism induces cardiac stress and systolic

Men Women

**Figure 1.** Left ventricular ejection fraction in men and women with congestive heart failure. *After Vasan, et al.1999*.

Heart failure arising from inadequate fluid return to the heart is most commonly experi‐ enced by women. It is well recognized that while half of heart failure patients are women [3], the characteristics of heart failure in women differ substantially from those observed in men. Specifically, heart failure develops later in life in women, is commonly associated with preserved systolic function (Figure 1) [4], less commonly involves ischemia, and, while sur‐

n = 40 n = 33

3 3 3

5

19

10

9

8

3

10

 >0.60 0.50-0.59 0.41-0.49 0.31 - 0.40 <0.30

hypertension, eventually leading to cardiomyopathy.

0

20

40

60

Percent

266 Cardiomyopathies

80

100
