Staging of Hypertensive Heart Disease.Precipitants and clinical sequelae related to LVH and myocardial fibrosis.Imaging in hypertensive heart disease .Differential diagnosis of LVH.Concentric LVH .Eccentric LVH . Concentric remodeling .linking hypertension and atrial fibrillation

1. Magdy El-Masry
Prof. of Cardiology
Tanta University

4. Hypertensive heart disease refers to heart conditions
caused by high blood pressure.
It’s not a single disease, but rather, a number of different
heart disorders all caused by the same thing :
the heart working under increased pressure

5. Left ventricular hypertrophy
Heart failure ( HFpEF & HFrEF )
Coronary artery disease
Arrhythmias : AF & PVCs
Careful attention and treatment of LVH, HF, CAD, and AF will improve survival.
Sudden
Cardiac
Death

6. Dzau V, Braunwald E. Resolved and unresolved issues in the prevention and treatment of
coronary artery disease: a workshop consensus statement. Am Heart J 1991;121:1244–1263.

7. Staging of Hypertensive Heart Disease
HFpEF
HFrEF

8. How High Blood Pressure Can Lead to Heart Failure ?
Role of RAAS

9. Physiological and detrimental roles of RAAS molecules
in cardiac, vascular tissues and kidneys.
Aldosterone and Ang II are the principal RAAS molecules involved in cardiovascular and renal system changes during
hypertension. Both molecules are also involved in the physiological control of blood pressure (blue text), directly
impacting cardiomyocytes, kidney epithelial cells, and vascular smooth muscle cells. During hypertension, excesses of
these molecules have also been linked with cardiovascular and kidney tissue hypertrophy and fibrosis (red text)

10. An imbalance in collagen metabolism
In hypertensive heart disease an excess of collagen is found in the extracellular matrix of
the myocardium. This is thought to be due to an imbalance in collagen metabolism
resulting from both increased synthesis as well as normal or reduced degradation.
PIP = carboxy-terminal propetide of procollagen type, PIIIP = carboxy-terminal propetide of
procollagen type III, CITP = carboxy-terminal telopeptide of collagen type I,
TIMP-1 = tissue inhibitor of matrix metalloproteinases type I.

11. Pathological changes of the left ventricle during long-term exposure to chronic pressure
overload include an increase in the size of the cardiomyocyte, alterations in the
extracellular matrix with accumulation of fibrosis, and abnormalities of the intramyocardial
coronary vasculature, including medial hypertrophy and perivascular fibrosis

12. Precipitants and clinical sequelae related to
LVH and myocardial fibrosis
Systolic BP
RAAS
LVH + Myocardial fibrosis→ a common end point in hypertensive heart disease

13. 3D Model of the Regional Changes in LV Geometry Associated With SBP
A long-axis section of the 3D CMR–derived fitted regression model taken at SBP of 100 mmHg (red filled
contour) and 180 mm Hg (black outline) shows how LV geometry varies between these 2 BP.
Arrows indicate the relationship between each coefficient and SBP.
JACC: Cardiovascular Imaging Volume 8, Issue 11, November 2015
left ventricular properties associated with increasing systolic blood pressure
SBP of 180 mmHg
SBP of 100 mmHg

14. Advantages and disadvantages of the various methods currently available to assess LVH.
+ : Low ++ : Moderate +++ : High
Imaging in hypertensive heart disease : Left ventricular hypertrophy

16. Echocardiography : M-Mode

17. Echocardiography : 2D

18. Cardiac Magnetic Resonance

19. The prevalence and influenced age among the differential diagnosis of LVH.
LV hypertrophy − a disease of many faces
Curr Cardiol Rep (2017) 19: 65

20. Differential diagnosis of LVH : Cardiac Imaging

21. Differential diagnosis of LVH :Cardiac Imaging
Curr Cardiol Rep (2017) 19: 65

22. Understanding left ventricular hypertrophy

23. What is Left Ventricular Mass ( LVM ) and Relative Wall Thickness ( RWT ) and how do
we obtain these values?
→

24. Left Ventricular Mass ( LVM )
LVM (g) = 0.8 x 1.04 x [(IVSd + LVd + PWd)3 – LVd3] + 0.6g
Concentric LVH = increased LVM
Eccentric LVH = increased LVM
Concentric remodeling = normal LVM
Relative wall thickness (RWT) allows further classification of LV mass increase as
either concentric hypertrophy (RWT >0.42) or eccentric hypertrophy (RWT ≤0.42).

25. Relative Wall Thickness ( RWT )
 The RWT is calculated by doubling the dimension of the posterior wall and
dividing by the LV dimension. RWT = ( 2 x PWd ) / LVd
 Another variable of this equation would be to add the IVS and PW instead of
multiplying the PW by two. The reason this method is less preferred is
because septal measurements may be confounded by the presence of septal
bulge. RWT = (IVSd + PWd) / LVd
Concentric LVH = increased RWT
Eccentric LVH = decreased RWT
Concentric remodeling = increased RWT

26. Understanding left ventricular hypertrophy

27. Understanding left ventricular hypertrophy

28. Understanding left ventricular hypertrophy

29. Diagrammatic representation of the classification of left ventricular hypertrophy

30. Common and often co-existing cardiovascular conditions with
a risk for adverse events including sudden death.

31. Pathophysiology of hypertensive heart disease.
Note the similarity of manifestations of coronary artery disease and hypertensive heart disease.

32. Potential pathogenic mechanisms linking hypertension and atrial fibrillation.

33. Aetiology of ventricular arrhythmias in hypertension.

34. Some angiotensin II related effects of relevance for arrhythmogenesis
RAA system plays an important role for the control of LV mass and structure. Consequently,
recent interest has focused on ARB , because this class of drugs might interact with several
possible arrhythmogenic mechanistic factors induced by angiotensin II acting on type 1 receptor

35. Combined Hypertension and Heart Failure
Navigating Troubled Waters

36. Drug Compliance ( Medication Adherence )

37. Hypertension Heart Failure
HTN increases
the risk of HF by two or
three-folds and probably
accounts for about 25%
of all cases of HF.

40. Drugs for Hypertension
The A,B,C,D drug classes
Angiotensin-converting enzyme
inhibitors
Angiotensin receptor blockers
Beta-blockers
Calcium channel blockers
Diuretics
Treatment of HTN : First‐line drugs
In the absence of any compelling condition, any of the following three classes of
agents can be used as a first‐line therapy:
 Thiazide diuretic
 ACE‐I or ARB
 CCB

41. Core drug treatment strategy for uncomplicated hypertension
The core algorithm is also appropriate for most patients with
HMOD, cerebrovascular disease, diabetes, or PAD.

42. Drug treatment strategy for hypertension and CAD

43. Drug treatment strategy for hypertension and AF.
a Non-DHP CCB (non-DHP CCB, e.g. verapamil or diltiazem).
CHA2DS2-VASc = Cardiac failure , Hypertension, Age
≥75 (Doubled), Diabetes, Stroke (Doubled) – Vascular
disease, Age 65–74 and Sex category (Female)

44. Drug treatment strategy for hypertension and HFrEF.
Do not use non-dihydropyridine CCBs (e.g. verapamil or diltiazem)
a Consider an angiotensin receptor/neprilysin inhibitor instead of ACEi or ARB per ESC Heart
Failure Guidelines.
b Diuretic refers to thiazide/thiazide-like diuretic. Consider a loop diuretic as an alternative in
patients with oedema.
c MRA (spironolactone or eplerenone).

45. Therapeutic
algorithm for
a patient with
symptomatic HFrEF

48. Blood pressure paradox in patients with heart failure
The relationship between systolic blood pressure and cardiovascular disease events in
patients with heart failure
In patients with HFrEF, a low BP reflects not only a lower LV
systolic contractility but also a lower cardiac output.
Indeed, BP is low because the heart is unable to contract
normally (decapitated hypertension).
Therefore, a higher BP is associated with a decreased mortality
because, in patients with HF, BP may be an indirect measure of
LV function.
A higher SBP in patients with HF is associated with a paradoxically
protective effect on survival.
Several studies, have shown that in most HF populations, high and,
not as one would expect, low SBP is associated with improved
outcomes

49. Three main
pathophysiological
mechanisms
contribute to the
development of
flash pulmonary
edema:
1) defective
pressure
natriuresis with
sodium and fluid
retention;
2) Increased LVEDP
associated with
LVH and stiffening;
and 3) failure of
the pulmonary
capillary blood–gas
barrier.
Flash pulmonary
oedema and bilateral
renal artery stenosis:
The Pickering Syndrome

50. Flozins

52. What you need to know ?

53. Arterial Hypertension in Patients with Heart Failure
 HTN carries the highest population-attributable risk for HF together with CAD
, and as a comorbidity is present in most patients with HF.
 There is inter individual variability in the progression from HTN to HF in both
the geometry of LV growth and the level of EF.
 The assessment of the hypertensive failing heart must combine imaging and
biochemical markers of the structural and function alterations of the
myocardium.
 The prevalence of HF calls for prevention efforts, and arterial HTN is a prime
target for such interventions.
 Because arterial HTN may complicate HF , adding further morbidity and
mortality risk, its management influences the prognosis of patients with HF.

54. Suggested
Empirical
Antihypertensive
Strategy in HF
Patients With
Persisting
Hypertension