**5. Hypertension and ischaemic heart disease**

Hypertension is a well-recognised risk factor for CVDs [28]. In fact, 14 weeks of hypertension can increase left ventricular weight by 30% and wall thickness by 42%, while the number of myocytes and total length of capillaries remain constant. Hypertrophy of myocytes is associated with reduced mitochondria to myofibril ratio [29]. Thus, physiological and pathological cardiac hypertrophies are caused by different stimuli and functionally distinguishable. A pathological stimulus causing pressure overload like hypertension produces an increase in systolic wall stress which results in in concentric hypertrophy (a heart with a very thick wall but with relatively small cavities) [30]. In the pathological hypertrophied heart, the function may decompensate, resulting in left ventricle dilation and HF. However, in physiological hypertrophy, the function does not decompensate [30]. Accordingly, regular exercise training (ET) can induce beneficial effects in the myocardium. Cardiac action potential duration (CAPD) of the hypertrophied heart is prolonged compared to control [31]. According to literature, mortality rates from coronary artery and cerebrovascular diseases can increase progressively as blood pressure increases [21]. CAD is caused by the accumulation of lipid and inflammatory cells in the arterial walls to form atherosclerotic plaques. Unstable coronary plaques are prone to erosion or rupture, obstructing coronary blood flow and causing an acute myocardial infraction (MI). It is now known that **v**arious CVDs can alter the ultrastructure of the heart. Myocardial ischaemia develops when the coronary blood supply to the myocardium is reduced either in terms of absolute flow rate (low-flow or no flow) or relative to increased tissue demand. The main feature of ischaemia is that oxygen supply to the mitochondria is insufficient to support oxidative phosphorylation [32]. After the onset of ischaemia, ultrastructural changes in the myocardium occur rapidly. These changes can be considered as reversible alterations if reperfusion of the tissue can be effected quickly. However, when ischaemia lasts for more than 20–30 min without collateral flow, the result is a transition from

**101**

tissue biopsies from the left ventricle [45].

diseases.

*Inflammation and Diabetic Cardiomyopathy DOI: http://dx.doi.org/10.5772/intechopen.88149*

elevated diastolic [Ca2+]i [35].

**6. Diabetes induced cardiomyopathy (DCM)**

a state of reversible ultrastructural alterations to a state of irreversible tissue injury [33]. An early consequence of myocardial ischaemia is depression of myocardial contractility. Also during ischaemia, arrhythmias may occur, ranging in severity from isolated ventricular premature beats, through runs of ventricular tachycardia, to ventricular fibrillation [34]. During ischaemia, there is a reduced availability of oxygen and the metabolic substrates, leading to a deficit of high-energy phosphates. In addition, the Ca2+ uptake mechanisms in the sarcoplasmic reticulum (SR) of cardiac myocytes are impaired, leading to intracellular free Ca2+ accumulation or

CVDs are closely associated with diabetes-induced hyperglycaemia, resulting in the death in 80% of people with diabetes [1]. Diabetic cardiomyopathy (DCM) is defined as a disorder of the heart muscle caused by diabetes. It results in pathological cardiac remodelling without previous incidence of CAD, hypertension and valvular disease. The exact cellular, subcellular and molecular mechanisms of DCM are complex and remain unclear [2]. Thus, further studies are essential for better understanding of the mechanism(s) of DCM and also in reversing the pathological cardiac remodelling induced by diabetes [3]. The increased frequency of HF in diabetic patients can persist despite correction for age, obesity, hypercholesterolemia and CAD. DCM is characterized by diastolic dysfunction, which can lead to the development of systolic dysfunction [36]. Echocardiography for patients with type 1 diabetes mellitus (T1DM) without known CAD shows diastolic dysfunction with a reduction in early diastolic filling, increase in atrial filling, an extension of iso-volumetric relation and increased numbers of supra-ventricular premature beats. The most common abnormality observed in asymptomatic diabetics is left ventricular (LV) diastolic dysfunction, likely resulting from greater LV myocardial and vascular stiffness [37]. A deep understanding of its development is necessary for the early diagnosis and subsequent treatment of diabetes-related cardiovascular

There is a rapidly growing literature on DCM investigating the structural, functional and metabolic changes that occur in the diabetic myocardium and how these changes contribute to the development of DCM in humans [38, 39]. The structural changes include left ventricular hypertrophy, interstitial fibrosis, increased cell death and oxidative stress and myocardial lipotoxicity [40, 41]. The functional changes include diastolic dysfunction, systolic dysfunction and impaired contractile reserve. Metabolic changes include altered substrate utilisation and mitochondrial dysfunction [42]. In type 2 diabetes mellitus (T2DM), left ventricular mass is an independent marker of cardiovascular risks that often occur independently of atrial blood pressure. Hence, diabetes is an independent risk factor leading to left ventricular hypertrophy, myocardial stiffness and inflammation [43]. DCM is also characterized by interstitial fibrosis, mostly composed of collagen and perivascular fibrosis [44]. In biopsies from diabetic heart patients, the deposition of collagen around the vessel and between myofibres is significantly raised. Furthermore, lipofuscin (which is a brown pigment composed of lipid-containing residues), cholesterol and myocardial triglyceride is also significantly increased in cardiac

During DCM, hyperglycaemia (HG) can lead to both acute reversible cellular metabolism damage and irreversible changes in endogenous macromolecules in the heart [46]. Elevated blood HG can affect many organs in the body including the kidneys, the eyes, the nerves and the heart resulting in long-term damage and *Inflammation and Diabetic Cardiomyopathy DOI: http://dx.doi.org/10.5772/intechopen.88149*

*Inflammatory Heart Diseases*

and C-reactive protein (CRP) [25].

induced cardiomyopathy (DCM).

of athero-thrombotic complications. Baseline measurements of some inflammatory markers are well-known to be predictive risk factors for future CVD events in prospective epidemiological studies. Inflammatory markers dominant in the literature are acute phase response (APR)-associated, and they include fibrinogen

The presence of subclinical inflammation is accompanied by an elevated concentration of high-sensitivity CRP and increased concentrations of other inflammatory markers. Epidemiological studies suggest strong association between

There are a number causal risk factors which are associated with CVDs and it is of paramount importance to understand and recognise these risk factors in order to predict and more so, to prevent CVDs. Risk factors may be causal or just a marker of risk(s) in nature and they are often called "innocent bystanders" [26]. The WHO has identified high blood pressure, tobacco use, physical inactivity, unhealthy diet, overweight, obesity, diabetes, high blood glucose and high cholesterol, as the main causal factors of the global burden of CVDs [27]. This review will now focus on how hypertension and diabetes mellitus can lead to heart failure (HF) and diabetes-

Hypertension is a well-recognised risk factor for CVDs [28]. In fact, 14 weeks of hypertension can increase left ventricular weight by 30% and wall thickness by 42%, while the number of myocytes and total length of capillaries remain constant. Hypertrophy of myocytes is associated with reduced mitochondria to myofibril ratio [29]. Thus, physiological and pathological cardiac hypertrophies are caused by different stimuli and functionally distinguishable. A pathological stimulus causing pressure overload like hypertension produces an increase in systolic wall stress which results in in concentric hypertrophy (a heart with a very thick wall but with relatively small cavities) [30]. In the pathological hypertrophied heart, the function may decompensate, resulting in left ventricle dilation and HF. However, in physiological hypertrophy, the function does not decompensate [30]. Accordingly, regular exercise training (ET) can induce beneficial effects in the myocardium. Cardiac action potential duration (CAPD) of the hypertrophied heart is prolonged compared to control [31]. According to literature, mortality rates from coronary artery and cerebrovascular diseases can increase progressively as blood pressure increases [21]. CAD is caused by the accumulation of lipid and inflammatory cells in the arterial walls to form atherosclerotic plaques. Unstable coronary plaques are prone to erosion or rupture, obstructing coronary blood flow and causing an acute myocardial infraction (MI). It is now known that **v**arious CVDs can alter the ultrastructure of the heart. Myocardial ischaemia develops when the coronary blood supply to the myocardium is reduced either in terms of absolute flow rate (low-flow or no flow) or relative to increased tissue demand. The main feature of ischaemia is that oxygen supply to the mitochondria is insufficient to support oxidative phosphorylation [32]. After the onset of ischaemia, ultrastructural changes in the myocardium occur rapidly. These changes can be considered as reversible alterations if reperfusion of the tissue can be effected quickly. However, when ischaemia lasts for more than 20–30 min without collateral flow, the result is a transition from

high-sensitivity CRP concentrations and CVD risks [37].

**4. Risk factors for cardiovascular diseases**

**5. Hypertension and ischaemic heart disease**

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a state of reversible ultrastructural alterations to a state of irreversible tissue injury [33]. An early consequence of myocardial ischaemia is depression of myocardial contractility. Also during ischaemia, arrhythmias may occur, ranging in severity from isolated ventricular premature beats, through runs of ventricular tachycardia, to ventricular fibrillation [34]. During ischaemia, there is a reduced availability of oxygen and the metabolic substrates, leading to a deficit of high-energy phosphates. In addition, the Ca2+ uptake mechanisms in the sarcoplasmic reticulum (SR) of cardiac myocytes are impaired, leading to intracellular free Ca2+ accumulation or elevated diastolic [Ca2+]i [35].
