Hypertensive heart disease (HHD) is a term applied to refer to all cardiac pathological conditions which are directly or indirectly caused by high blood pressure.
The type of disease, its duration and its severity greatly affect the signs and symptoms of HHD. Hypertension is among the most important of these, and since many patients might not be aware of its presence, hypertension is frequently referred to as the “silent killer”.
Patients are generally asymptomatic, except in the cases when LVH is pronounced enough to be able to lead to diastolic dysfunction and heart failure.
Symptomatic diastolic heart failure and systolic heart failure can be hard to distinguish due to the similarity of their symptoms, thus the study of the patient’s medical history is paramount. Particular attention should be given to the cases characterized by rapid CHF appearance followed by rapid return to the baseline, a situation more closely related to diastolic dysfunction. Other heart failure symptoms include:
In addition to these, pulmonary edema can also occur due to the sudden decomposition in the LV systolic and diastolic dysfunction, which is turn is caused by a series of precipitating factors like acute rise of the blood pressure, myocardial ischemia, and dietary indiscretion. Cardiac arrhythmia (especially atrial fibrillation) and heart failure can also occur.
It is particularly difficult to distinguish angina, one of the most frequent HHD complications, from other etiological factors of myocardial ischemia. Among the most frequently reported angina symptoms there is substernal chest pain lasting for less than 15 minutes (contrarily to what happens in infarction, where substernal chest pain lasts for more than 20 minutes). The classical features of the pain reports are indicated as follows:
Atypical symptoms without chest pain might also occur, such as exertional dyspnea or excessive fatigue, and their appearance is particularly frequent in women. Patients might present chronic and stable angina or acute coronary syndrome. In the cases of hypertensive crisis ischemia ECG changes can be detected, even though no significant coronary atherosclerosis can be observed. The sudden rapture of an atherosclerotic plaque might precipitate an acute coronary attach, but this can also be caused by a marked increase of the blood pressure responsible for a sudden rise of transmural pressure with no effect over the plaque stability.
A series of symptoms appear in the cases of irregular or abnormal heart rhythm, which can be summed up as follows:
The predominant cardiac abnormality and the duration and severity of HHD greatly influence the HHD physical signs. The findings might be absent upon physical examination in the early stages of the disease. Physical examination can also detect the clues of a potential hypertension etiology, like abdominal mass in polycystic kidney disease, renal artery bruit in renal artery stenosis, and truncal obesity and striae in Cushing syndrome.
While arterial pulses appear normal in the early phases of HHD, cardiac rhythm appears regular in sinus rhythm and irregular in atrial fibrillation. The general features of the heart rate can be summed up as follows:
Generally speaking, the pulse volume is normal, even though it can be decreased when LV dysfunction appears. If coarctation of the aorta is the hypertension etiological factor, radial-femoral delay can be observed.
The blood pressure is elevated in both the systolic and diastolic phase, with a maximum value greater than 140 mmHg and the minimum one greater than 90 mmHg. In the cases of coarctation of the aorta, the blood pressure appears higher when measured at the higher extremities than the lower extremities. In any case, the value of blood pressure is normal if the patient has received a proper antihypertensive treatment or, due to the advanced phase of LV dysfunction, the heart can no longer guarantee the generation of a sufficient cardiac outcome to produce high levels of blood pressure.
Jugular veins might appear distended in the cases of heart failure, which it turn, together with other associated lesions, might affect the predominant waves. In the cases characterized by LVH but without significant systolic LV the apical impulse appears sustained and not displaced. The apical impulse displaces laterally due to LV dilatation when significant systolic LV dysfunction occurs in a later stage of the disease. If significant pulmonary hypertension is present, a lift in the right ventricle might appear later during the heart failure.
While S1 appears normal both in terms of intensity and character, S2 becomes loaded along the right upper sternal border due to the marked aortic component (A2). Furthermore, S2 might have a reverse or paradoxical split as a consequence of the increased afterload or the related left bundle-branch block. S3 is generally not present in the early stages of the disease, but becomes audible when heart failure occurs. Contrarily, S4 often appear well palpable and audible, something which underlines the presence of a stiffened and noncompliant ventricle following the chronic pressure overload and LVH.
Diastolic murmur of aortic insufficiency can be heard very early along the mid/left parastemal area, particularly when acutely elevated blood pressure occurs. It then often disappears once the blood pleasure is yet again under control. A systolic to midsystolic murmur of the aortic sclerosis can also be heard in a early stage of the disease, while a holosystolic murmur of the mitral regurgitation is frequently observed in the cases of advanced heart failure and dilated mitral annulus.
Upon chest examination, clinical findings frequently appear normal and might include clues of pulmonary congestion like rales, decreased breath sounds, and a dullness to percussion following pleural effusion. In the cases of hypertension due to renal artery stenosis, renal artery bruit can be revealed after abdominal examination, together with a pulsative expansible mass of abdominal aortic aneurysm and ascites/hepatomegaly following an episode of CHF.
The classical sign which involves extremities is the appearance of edema at the level of ankles in the cases of advanced heart failure. No major CNS findings can be detected, unless the patient concerned has experienced previous episodes of cerebrovascular accidents which have left residual physiologic deficit. CNS changes can frequently be seen in those patients in hypertensive crisis. Upon fundi examination, hypertensive retinopathy might be revealed, whose severity depends on the hypertension duration and severity.
According to the 7th Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure, the following baseline laboratory tests are recommended in the evaluation of HHD:
Cardiovascular risk assessment
With its guideline released in 2013, the American Heart Association/American College of Cardiology (AHA/ACC) recommends a revised calculator to measure the 10-years risk of first atherosclerosis cardiovascular disease (ASCVD) event. This is defined as the occurrence in a person with no initial ASCVD risk of nonfatal myocardial infarction, death from coronary disease, and stroke. The calculator requires the use of clinical and laboratory risk factors, such as hypertension treatment and systolic blood pressure , as well as diet and physical activity . In the cases with elevated 10-year risk, clinicians are recommended to communicate data risk regarding blood cholesterol  and obesity  to AHA/ACC guidelines.
The treatment for HHD can be divided in two main categories: treatment for the elevated blood pressure and treatment for HHD itself. The treatment goals should be as indicated below :
According to recent data, to reduce the risk of congestive heart failure by at least 64%, the target blood pressure in patients older than 80 years of age should be 150/80mm Hg . Other possible treatment strategies include:
It should be remembered that an efficient treatment of HHD requires the involvement of different professionals with different fields of expertise, such as preventive cardiologists, heart failure specialist and electro-physiologists.
The mortality and morbidity rate of HHD appear to be higher than those observed in the general population and their value is dependent to the specific cardiac pathology concerned . The data collected so far seem to indicate that the increase in the mortality and morbidity rates is due more to the pulse pressure than the absolute systolic or diastolic blood pressure, even through both of them are important in the evaluation of HHD.
The etiology of HHD can be seen as a complex interaction of several elements working together, which include hemodynamic, neuroendocrine, structural, cellular, and molecular factors . All these factors are very important in the process of hypertension development, but they are all modulated by high levels of blood pressure.
All in all, elevated levels of blood pressure can influence the cardiac structure directly by increasing afterload or indirectly by inducing related neurohormonal and vascular changes. In particular, it has been shown that the changes most closely related to the cardiac pathologies indicated above are those due to elevated 24-hour ambulatory blood pressure or nocturnal elevated blood pressure, a trend which has been especially observed in people with African origin.
It is interesting to note that obesity has been linked to hypertension and LVH in many epidemiological studies, with at least 50% of obese subjects suffering from hypertension and at least 60-70% of hypertension subjects being obese. For this reason, obesity has to be seen as another risk factor for the development of HHD.
In 2005 the prevalence of hypertension in the United States has been estimated to be 35.3 millions in men and 38.3 millions in women. The prevalence appears to be higher in people with African origin than people with a Hispanic or non-Hispanic white background, and its value over the last decades has been characterized by a marked increase. For example, according to the data collected between 1988 and 1994 or 1999 and 2002, the prevalence of hypertension in people with African origin has increased from 35, 8% to 41.4%, and this trend can also be seen among people with a white background, although not with the same intensity . It should be noted that this difference is not due to race but to other factors, since similar studies conducted in United Kingdom show the same hypertension prevalence among black and white people and hypertension itself is quite rare in the African continent.
Age is responsible for the increase of systolic blood pressure, even through this increase is more marked in women than men due to the effects of menopause which greatly increases the levels of blood pressure. Generally speaking, the prevalence of hypertension is higher in men than women when considering people under 55 years of age, but higher in women than men when considering people above 55 years of age. It is very probable that the prevalence of HHD follows the same trend. According to the data collected from ECG findings, the frequency of LVH is low, being 2.9% in women and 1.5% in men. However, this rate appears to be much higher when considering the data coming from echocardiographic findings, with a value ranges from 15% and 20%.
An increased amount of work results from the development of myocytic hypertrophy. The thickened myocardium then reduces the compliance of the left ventricle, which in turn impairs diastolic filling. The direct consequence of the myocyte hypertrophy is the increased distance for oxygen and nutrient diffusion between neighboring capillaries. It is interesting to note that in a great number of patients hypertension is followed by coronary atherosclerosis, and this might subsequently lead to the development of ischemia.
As a consequence of all this, marked changes can be observed on the heart structure. The left ventricle wall appears thickened, and this is accompanied by an increase in the heart weight. In fact, in normal conditions, the heart weight ranges between 500 and 600 grams, but in hypertensive conditions it might reach 1100 grams. Furthermore, the papillary muscle and the so called trabeculae carneae become rounded and more prominent, and this to the detriment of the volume of the cardiac chamber which appears to be much smaller as a consequence of its hypertrophic growth called “concentric hypertrophy”. In this condition, if cardiac failure occurs, the dilatation chamber is also more prominent. The effect of the long-lasting hypertension might be the development of endiocardial fibrous thickening in the left ventricle, and if left ventricular failure also occurs dilatation and hypertension appear on the heart right side.
From a cytological point of view, it is possible to observe a marked enlargement of myocytes and nuclei. Furthermore, while the left ventricle chamber is dilating and the wall is thickening, interstitial fibrosis, focal myocyte atrophy and focal myocyte degeneration begin to develop. In the cases of malignant hypertension, it is also possible to observe the appearance of myocardial edema and necrosis foci which are characterized by either intense eosinophilia or complete muscle fiber dissolution.
Since HHD symptoms might appear without the patient being aware of them, frequent measurements are recommended. Symptoms often appear after many years of no blood pressure control or when a sudden marked increase occurs. Recommended measurement frequencies are every 2 years if blood pressure is lower than 120/80mm Hg at the time of the most recent reading, or once a year if it is 120-139/80-89 mmHg.
Blood pressure is an important factor for the heart physiology and its changes might greatly affect the heath structure, its conduction system, and the coronary vasculature. This is the reason why pathological changes in blood pressure might lead to the development of important cardiac diseases such as left ventricular hypertrophy (LVH), coronary heart disease (CAD) systolic and diastolic dysfunctions, several conduction system diseases, or a whole host of other complications such as angina, myocardial infarction, cardiac arrhythmias (in particular atrial fibrillation), and congestive heart failure (CHF). The term hypertensive heart disease (HHD) has been defined to refer to this series of related cardiac diseases and complications which, as mentioned previously, are ultimately caused directly or indirectly by marked changes and elevated levels of blood pressure. These diseases generally manifest themselves in the case of chronically elevated blood pressure, but cases of marked or acute blood pressure can still have an effect on them by increasing the underlying predisposition to their development at some point during lifetime. For the purposes of differential diagnosis, the following conditions should also be taken into consideration during the evaluation of HHD:
The term “hypertensive heart disease” refers to all those pathologies which occur because of elevated blood pressure. These might include:
In high blood pressure conditions, the heart pumps against this high pressure and therefore has to work harder to obtain the same cardiac outcome. Over the time this situation causes the heart to thicken and to reduce the volume of the cardiac chamber. If this condition is not timely treated, the symptoms of HHD begin to appear. Heart failure might develop, and frequently heart walls can become so thick that the heart itself can no longer pump a sufficient quantity of oxygen. This in turn provokes chest pain, in a condition called angina.