This document discusses the effects of hypertension on vessels and the heart. It defines various types of hypertension and their causes. Essential or primary hypertension accounts for 95% of cases and results from genetic and environmental factors that increase blood volume and peripheral resistance. This causes pathological changes in vessels like hyaline arteriolosclerosis and hyperplastic arteriolosclerosis. Hypertension can also lead to hypertensive heart disease, causing left ventricular hypertrophy and eventually heart failure if not controlled. Pulmonary hypertension from lung diseases can cause right ventricular hypertrophy known as cor pulmonale. Long term hypertension increases the risks of stroke, heart disease, and renal failure.

1. Effects of Hypertension on
Vessels and Heart
2020

2. LOs
• Mention types of hypertension.
• Enlist causes of secondary hypertension.
• Know the pathogenesis of pathological effects of hypertension on
heart and vessels.
• Describe the pathological changes in the heart and vessels due to
hypertension.
• Know the outcome of hypertension.

3. Hypertension (HTN)
Hypertension; an elevation in blood pressure (B.P) beyond normal values of
120/80 mmHg.
Sustained diastolic pressures greater than 90 mm Hg or sustained systolic
pressures in excess of 140 mm Hg are reliably associated with an increased
risk for atherosclerosis and are therefore used as cutoffs in diagnosing
hypertension in clinical practice.
Three forms of hypertension
Systemic
Pulmonary
Portal

4. Systemic HTN
Types of Systemic Hypertension:
Essential (Primary) HTN
Secondary HTN
Malignant hypertension;
Approximately 5% of hypertensive patients (when systolic B.P = 200 mm and
diastolic B.P is above 120 mmHg ), if untreated, leads to death in within 1 to 2
years.
Malignant hypertension is frequently associated with renal failure and retinal
hemorrhages, with or without papilledema.
It may develop in previously normotensive persons but more often is superimposed
on preexisting benign hypertension, either essential or secondary.

5. Essential (Primary) HTN
Essential (idiopathic) HTN (95% of cases)
Gradual age-associated rise in B.P “essential” for normal perfusion of end
organs such as the brain.
Pathogenesis:
Specific triggers unknown
However essential HTN results from the interplay of several genetic
polymorphisms and environmental factors, which alter renal sodium
handling, increase blood volume and /or peripheral resistance.

6. Essential (Primary) HTN
Mechanisms
Reduced renal sodium excretion (probably a key pathogenic feature);
In the presence of normal arterial pressure; decrease sodium excretion
causes an obligatory increase in fluid volume and increased cardiac output,
thereby elevating B.P. At the new higher B.P, the kidneys excrete additional
sodium. Thus, a new steady state of sodium excretion is achieved, but at the
expense of an elevated B.P
Increased vascular resistance; may stem from chronic vasoconstriction
may result in permanent thickening of the walls of affected vessels.
Genetic factors; play an important role in determining B.P, as shown by
familial clustering of hypertension. In a small proportion of cases of essential
hypertension there is linkage to specific angiotensinogen polymorphisms
and angiotensin II receptor variants
Environmental factors; Stress, obesity, smoking, physical inactivity, and
high levels of salt consumption, modify the impact of genetic
determinants.

8. Essential HTN
Risk Associated with Essential HTN:
Essential HTN is compatible with long life unless following complication
supervenes.
1. Stroke
2. Hypertensive heart disease (coronary heart disease, cardiac hypertrophy
and heart failure)
3. Aortic dissection
4. Multi-infarct dementia
5. Renal failure
(Without appropriate treatment, some 50% of hypertensive patients die of
ischemic heart disease (IHD) or congestive heart failure, and another third
succumb to stroke)

9. Secondary HTN
Secondary HTN: with known causes
Pathogenesis: Most of the cases are due to;
Primary renal disease
Renal artery narrowing (renovascular hypertension)
Adrenal disorders
Single-gene disorders affecting renal sodium resorption, several relatively
rare disorders include the following:
• Gene defects in enzymes involved in aldosterone metabolism
• Mutations in proteins that affect sodium resorption
Prognosis: Depends on adequate treatment of the underlying cause.

10. Causes of Secondary HTN
RENAL
Acute
glomerulonephritis
Chronic renal disease
Polycystic disease
Renal artery stenosis
Renal vasculitis
Renin-producing
tumors
CARDIOVASCULAR
Coarctation of aorta
Polyarteritis nodosa
Increased intravascular
volume
Increased cardiac output
Rigidity of the aorta
NEUROLOGIC
Psychogenicnial
pressure
Sleep apne
Increased intracraa
Acute stress, including
surgery
ENDOCRINE
Adrenocortical hyper function
(Cushing syndrome, primary aldosteronism,
congenital adrenal hyperplasia, licorice
ingestion)
Exogenous hormones
(glucocorticoids, estrogen [including
pregnancy-induced and oral contraceptives],
sympathomimetics and tyramine-containing
foods, monoamine oxidase inhibitors)
Pheochromocytoma
Acromegaly
Hypothyroidism (myxedema)
Hyperthyroidism (thyrotoxicosis)
Pregnancy-induced (pre-eclampsia)

11. Vascular Pathology in Hypertension
Injury to the vessel wall and in particular to ECs is the fundamental basis.
Injurious stimuli may be biochemical, immunologic, or hemodynamic.
The integrated function of ECs and the underlying SMCs is critical for the
vasculature to respond to various stimuli; such responses can be adaptive
or may lead to pathologic lesions.
Thus, EC injury or dysfunction contributes to a host of pathologic processes
including thrombosis, atherosclerosis, and hypertensive vascular lesions.
Ensuing SMC prolifération and matrix synthesis can help to repair a
damaged vessel wall, but also can eventually lead to luminal occlusion.
In addition to accelerating atherogenesis, hypertension-associated
degenerative changes in the walls of large and medium arteries can
potentiate both aortic dissection and cerebrovascular hemorrhage.

12. Stereotypical response to vascular injury
Intimal thickening,
emphasizing intimal smooth
muscle cell migration and
proliferation associated with
extracellular matrix
synthesis.
Intimal smooth muscle cells
may derive from the
underlying media or may be
recruited from circulating
precursors
3. Elaboration of
extracellular matrix
2. SMCs mitosis
1. Recruitment of SMCs or
smooth muscle precursor
cells to the intima

13. Arteriolosclerosis
A form of cardiovascular disease involving hardening and loss of elasticity of
arterioles or small arteries, most often associated with HTN & D. mellitus.
Arteriolosclerosis is the term used to describe 3 morphologic forms of
vascular disease affecting arterioles and small muscular arteries. These are:
1. Hyaline arteriolosclerosis,
2. Hyperplastic arteriolosclerosis
3. Necrotizing arteriolitis
All the three types are common in hypertension but may occur due to other
causes as well.
Arteriosclerosis: thickening, hardening and loss of elasticity of the walls
of arteries

14. Hyaline arteriolosclerosis
Chronic hemodynamic stress in benign HTN induces; leakage
of plasma components across injured ECs into vessel walls &
increased ECM production by SMCs leads to homogeneous,
pink hyaline thickening of arteriolar walls & luminal narrowing.
Vessels of older adult patients (normotensive or hypertensive)
show same changes but in hypertensive patient hyaline
arteriolosclerosis is more generalized and severe
Similar lesions also common in diabetic microangiopathy;
etiology is hyperglycemia-associated EC dysfunction.
In the kidneys of hypertensive, arteriolar narrowing caused by
hyaline arteriosclerosis leads to diffuse vascular compromise,
ischemic atrophy and nephrosclerosis (glomerular scarring)

15. Hyperplastic arteriolosclerosis
Hyperplastic arteriolosclerosis is more typical of
severe hypertension.
Vessels exhibit “onion skin,” concentric, laminated
thickening of arteriolar walls and luminal
narrowing.
The laminations consist of SMCs and thickened,
reduplicated basement membrane.
In malignant hypertension, these changes
accompanied by fibrinoid deposits and vessel wall
necrosis (necrotizing arteriolitis), particularly
prominent in the kidney.

16. Hypertensive Heart Disease (HHD)
• Systemic (left sided) HHD
• Pulmonary (right sided) HHD

17. Systemic (left sided) HHD
Basics for Diagnosis:
History of hypertension
Left ventricular hypertrophy in the absence of other causes
accounting for hypertrophy
The stimulus for hypertrophy is pressure overload

18. Systemic (left sided) HHD
Stages of HHD
Compensated HHD: With hypertrophy an adequate cardiac output is
maintained.
Decompensated HHD: Thickness of muscle wall increase demand for
oxygen, decrease compliance, and role of hypertension on atheroma, all
contribute to decompensated HHD and eventual dilatation.

19. Systemic (left sided) HHD
Gross:
Compensated stage - Concentric ventricular hypertrophy
Decompensated stage - Ventricular dilatation
(In both stages, heart weight increased)
Note: Left atrial dilation due to stiffening of the left
ventricle and impaired diastolic relaxation, leading to
atrial volume overload
Microscopy:
Large cardiac muscle fibers with large nuclei, later
interstitial fibrosis.

20. Systemic (left sided) HHD
Outcome of HHD:
• CHF
• Increased risk of sudden cardiac death
• Renal disease
• Stroke
Note: Drug control leads to regression of hypertrophy.

21. Pulmonary (right sided) HHD - Cor pulmonale
Pulmonary hypertension caused by primary disorders of the lung
parenchyma or pulmonary vasculature ends up in Cor pulmonale which
consists of;
Right ventricular hypertrophy
Right ventricular dilation
Generally, right ventricular dilation and hypertrophy caused by congenital
heart disease or by left ventricular failure are excluded by this definition.

22. Pulmonary (right sided) HHD - Cor pulmonale
Types of Cor pulmonale:
Acute cor pulmonale:
Most commonly follows massive pulmonary embolism with obstruction of
>50% of the pulmonary vascular bed.
Chronic cor pulmonale:
Occurs secondary to prolonged pressure overload caused by obstruction of
the pulmonary vasculature, or compression or obliteration of septal
capillaries (resulting from emphysema, interstitial pulmonary fibrosis, or
primary pulmonary hypertension).

23. Pulmonary (right sided) HHD - Cor pulmonale
Acute cor pulmonale
Right ventricle usually dilated but does not show
hypertrophy; if an embolism causes sudden death
the heart may even be of normal size.
Chronic cor pulmonale
Right ventricular (and often right atrial) hypertrophy.
In extreme cases the thickness of the right
ventricular wall may be comparable to or even
exceed that of the left ventricle.
When ventricular failure develops the right ventricle
and atrium may also be dilated. Such dilation may
mask right ventricular hypertrophy.

24. References
• Robbins Basic Pathology 10th edition Chapter 10 &11
pages 361 to 440