Hypertension and Hypertensive Heart Disease - PDF

Systemic Hypertension and Hypertensive Heart Disease Prof. Dr. Beste Ozben Sadic Marmara University School of Medicine Department of Cardiology  Learning Objectives  Definition of blood pressure  Definition of hypertension  Hypertensi...

Systemic Hypertension and Hypertensive Heart Disease Prof. Dr. Beste Ozben Sadic Marmara University School of Medicine Department of Cardiology  Learning Objectives  Definition of blood pressure  Definition of hypertension  Hypertension mediated organ damage  General approach to hypertensive patients  Diagnosis  Tests  Treatment 2  Blood Pressure  Arterial blood pressure – systemic blood pressure  the pressure exerted by circulating blood upon the walls of blood vessels  one of the principal vital signs.  Amount of circulating blood ???  5l/min, 300 l/hr, 7.200 l/day, 2.628.000l/yr,  X 70years = 183.960.000 lt. 3  Blood Pressure Which one of the physiological components of below palys a role in blood  There are two major physiological components pressure determination of blood pressure:  a static component, mainly determined by peripheral resistance  a pulsatile component, which depends on aortic elastic properties. 4  Both components are regulated by a number of physiological pathways, including  renal (sodium: volume homeostasis),  neural (sympathetic nervous system),  hormonal [renin– angiotensin–aldosterone system (RAAS)], and others)  vascular mechanisms. 5  Hypertension  Arterial hypertension – systemic hypertension  Persistently high blood pressure (BP) in systemic arteries is the hallmark of hypertension.  Increase in either systolic or diastolic blood pressure (or both)  Normal BP ? Optimal BP? Elevated BP? 6 7  Hypertension  Elevated blood pressure Optimal 120 / 140 / >90* *All units in mmHg 9 10 11 12 Hypertension 13 14 Modifiable Risk Factors of CAD  Hypertension  Hypertension is the most important modifiable risk  Diabetes factor for all-cause  Dyslipidemia morbidity and mortality globally.  Obesity  Tobacco Smoking  Sedentary Lifestyle – Physical Activity  Stress  Emerging Risk Factors  Hypertension  associated with three to four times increased risk for  Coronary artery disease,  Acute coronary syndrome,  Heart failure (mostly HF with preserved LVEF),  Atrial fibrillation,  Stroke,  Peripheral artery disease,  Renal failure… 16 17 Pathophysiology of elevated blood pressure and hypertension  Most patients with hypertension have essential or primary hypertension (the exact cause remains unknown)  An estimated 10% have secondary hypertension, with an identifiable cause (ex: renal or endocrine problems) 18  Pathophysiology of elevated blood pressure and hypertension  The pathophysiology of hypertension involves complex interactions between environmental and behavioural factors, genes, hormonal networks, and multiple organ systems (renal, cardiovascular, and central nervous system).  Vascular and immune mechanisms are also involved.  Dysregulation of these processes leads to hypertension, which if uncontrolled, can lead to hypertension-mediated organ damage (HMOD) and adverse CVD outcomes. 19  Figure 1 Pathophysiology of elevated blood pressure and hypertension. Eur Heart J, ehae178, https://doi.org/10.1093/eurheartj/ehae178  Renal Mechanisms  The kidneys are a key regulator of BP, and impaired renal function leads to hypertension.  The most important renal mechanisms for BP control are the pressure–natriuresis relationship and the RAAS.  The pressure– natriuresis relationship reflects the ability of kidneys to balance urinary sodium excretion with dietary sodium intake to maintain a normal BP.  In healthy subjects, the RAAS is activated by low sodium intake, stimulating renal sodium reabsorption and preserving intravascular volume and BP. High sodium intake leads to suppression of the RAAS to facilitate natriuresis. 21  Renal Mechanisms  Chronic activation of the RAAS shifts the pressure– natriuresis curve to the right, with higher BP values required to excrete an equivalent sodium load.  Angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) shift the curve to the left, reducing BP values necessary for effective natriuresis.  Impaired tubular ion transport leads to the development of salt-sensitive hypertension and excessive sodium and volume retention.  Renal vasoconstriction can lead to renal ischaemia, which stimulates inflammation and local generation of reactive oxygen species; these factors contribute to microvascular remodelling, arteriolar damage, impaired sodium excretion, and ultimately, hypertension. 22 23 Regulating Blood Pressure: The Renin- Angiotensin-Aldosterone System Primary- Adrenal adenoma, hyperplasia ↑ Aldosterone ↓ Renin Secondary- CHF, Renal disease, Pregnancy ↑ Renin ↑ Aldosterone Autonomic nervous system activities 25  Vascular Mechanisms  Structural and functional changes in small and large arteries are involved in the pathophysiology of hypertension.  Peripheral vascular resistance is mainly controlled Main resistant at the level of small arteries and arterioles structures of circulation are arteriols. (diameter < 250 μm) by the sympathetic nervous system, humoral factors, and local autoregulation.  Endothelial dysfunction and vascular remodelling are early hallmarks of hypertension and target- organ damage. What are the fist simgs of hypertension brfore organ These vascular alterations both initiate and damge  maintain hypertension and, therefore, are both a cause and consequence of high BP 26 Activities of vascular endothelium Atrial natriuretic peptide sodium and water excretion KIDNEY 27  Causes of Hypertension Essential hypertension 92-94% Secondary hypertension 6-8% Renal 4-5% Miscellaneous ~2% Endocrine 1-2%  Secondary hypertension due to renal disorders – Chronic pyelonephritis – Acute and chronic glomerulonephritis – Policystic kidney disease – Renal artery stenosis – Arterial nephrosclerosis – Diabetic nephropathy – Renin secreting tumors  ENDOCRINE CAUSES OF HYPERTENSION 1. ADRENAL DEPENDENT CAUSES Pheochoromocytoma Primary aldosteronism Hyperdeoxycorticosteronism Congenital adrenal hyperplasia(11β hydroxylase/17α hydroxylase deficiency) Deoxycorticosterone producing tumor Primary cortisole resistance Cushing syndrome 2. AME/11β –HSD DEFICIENCY  Genetic Type I AME Acquired Licoriche or carbenoxolone ingestion (Type I AME) Cushing syndrome (Type II AME) 3. THYROID DEPENDENT CAUSES  Hypothyroidism  Hyperthyroidism 4. PARATHYROID DEPENDENT CAUSES  Hyperparathyroidism 5. PITUITARY DEPENDENT CAUSES  Acromegaly  Cushing disease  REVERSIBLE IRREVERSIBLE Renal Renal  Renal Artery Stenosis  Chronic Renal Failure  CRF due to Pyelonephritis  Polycystic Renal Disease  Acute renal disease  Renal Paranchimal disease  Hydronephrose Monogenic syndromes  Renin produce tumors  Gitelman Endocrine  Liddle Vascular  Barter syndrome  AC  Vasculitis  PAN  Scleroderma  Takayasu Arteritis Iatrogenic Toxic  Glucocorticoids, NSAID, Decongestants, Liquorice, alcohol  Essential Hypertension Essential  Onset in 30s and 40s  Gradual onset  Gradual progression of HTN/slow addition of medications  Lack of severe end-organ damage  Family history  Often associated with obesity  Lack of signs and symptoms of secondary causes  Lack of laboratory evidence of secondary causes  Secondary Hypertension  Hypertension onset at age extremes 50  Lack of family history  Refractory - resistant hypertension  Rapid onset of severe hypertension  More severe HT mediated organ damage  Grade III/IV retinopathy, LVH/CHF, CKD  Sign and symptoms of secondary etiologies  Laboratory evidence of secondary etiologies  Clinical consequences of elevated blood pressure and hypertension  Longstanding hypertension causes organ damage and ultimately leads to cardiovascular, cerebrovascular, and clinical renal disease, which are all major contributors to the global burden of chronic disease.  Evidence of HMOD usually indicates long-standing elevated BP and/ or hypertension and confers incremental prognostic information regarding CVD risk in all BP categories.  Unless treated, HMOD can progress from asymptomatic to symptomatic, ultimately resulting in overt CVD events. 34 35 Hypertensive Mediated Organ Damage  Heart – Hypertensive heart disease  Vasculature  Peripheral arteries – carotid artery, femoral artery, abdominal aorta….  Brain  Kidneys  Eyes  Both structural and functional changes due to HT  may be different in men and women (for instance, left ventricular hypertrophy and left atrial dilatation are more frequent in women.)  BLOOD PRESSURE MEASUREMENT Korotkoff sounds: These sounds appear and disappear as the blood pressure cuff is inflated and deflated.  Systolic BP: arterial BP during systole (maximum arterial pulsatile pressure). This is measured using an auscultatory device at the onset of the first Korotkoff sound.  Diastolic BP: arterial BP during diastole (minimum arterial pulsatile pressure). This is measured using an auscultatory device at the time of complete disappearance of the Korotkoff sounds (fifth sound). If there is no disappearance of sounds (no fifth sound) then the fourth Korotkoff sound (muffling) is used to estimate diastolic BP. 37 38 39 Inter-arm difference: systolic BP difference of >10 mmHg when BP is measured sequentially in each arm 40 Postural/orthostatic hypotension: decrement of ≥20 mmHg in systolic BP and/or ≥10 mmHg in diastolic BP when BP is measured in the standing position at 1 and/or 3 min after standing following a 5-min period in the sitting or lying position. 41  BLOOD PRESSURE MEASUREMENT Automated (unattended) office BPM Improved reproducibility Seated alone, unobserved White coat effect can be reduced Office BP: can be measured manually or using an automated device. In addition, automated office BP (AOBP) can be conducted in a setting attended by a healthcare professional or in an unattended fashion. White-coat hypertension: BP that is above the threshold for diagnosing hypertension in the office but below the threshold in home/ ambulatory settings, e.g. ≥140/90 mmHg in office but