Syndrome X 6.4.07 For Selam Part C - Presentation Transcript
Home is where the heart is,
Friendship is a guest, a book, a fire,
a hand clasp, a place where souls
can rest
Nicotine Has Many Deleterious Effects on the CVS NICOTINE Kannel WB. J Hypertens 1990. McGill HC Jr. Am Heart J 1988. Robertson D. Am Heart J 1988. Catecholamines Vasopressin Thromboxane B 2 Prostacyclin, NO Blood pressure Heart rate Myocardial ischemia Arrhythmia HDL Triglycerides LDL Fibrinogen Platelet aggregation Hyperlipidemia Hypercoagulable state
ADVICE IS LIKE KISSING:IT COSTS NOTHING AND IT IS A PLEASANT THING TO DO -GEORGE BERNARD SHAW
MONEY WALKS-NOBODY TALKS!!!! It is said that for money you can have everything but you can buy food, not appetite you can buy books,not knowledge you can buy medicine,not health !!!
Insulin’s actions in normal humans and in obese hypertensives Normal Human Insulin Obesity or Hypertension Insulin Sympathetic Activation Vasodilation Increased Blood Pressure Decreased Blood Pressure No Increase in Blood Pressure Elevated Blood Pressure Potentiated Sympathetic Activation Attenuated Vasodilation Augmented Pressor Action Impaired Depressor Action Clinical Hypertension, 7th ed., Kaplan NM.
Diurnal blood pressure variation Am J Hypertens 2005; 18: 149-151.
What is morning BP surge?
The morning BP surge (MBPS) is calculated as the mean systolic BP during the 2 h after waking minus the night time lowest BP (mean systolic BP during 1 h that included the lowest sleep BP)
The Surge group MBPS > 45 mm Hg
Non-Surge group MBPS < 45 mm Hg
Am J Hypertens 2004;17:668-675.
Classification of nocturnal dippers
Percentage of nocturnal systolic BP reduction is calculated as (100 x {1-Sleep systolic BP/Awake systolic BP})
Patients are classified based on above value as
Extreme dippers if nocturnal systolic BP reduction was ≥ 20%
Dippers if decrease is ≥ 10% but <20%
Non-dippers if decrease is ≥ 0% but <10%
Risers if it is <0%
Am J Hypertens 2005; 18: 1528-1533
Symp. Activity (alpha adrenergic activity) Baroreceptor sensitivity RAAS activity Plasma cortisol, catecholamine levels MBPS Thromboembolic tendency Platelet aggregation Hematocrit Fibrinogen, PAI-1 Blood viscosity Hypercoagulability Fibrinolytic activity Impaired endothelial function NO production atherosclerosis Shear stress on vascular wall Vascular tone Cardiovascular events MI Sudden cardiac death Ventricular fibrillation Ventricular tachyarrhythmia Stroke Target organ damage Hypertension 2005;45:485-86 AJH 2005; 18: 145-181
Laragh’s pearls Am J Hypertens 2001; 14: 491–503.
CAFÉ - an ASCOT substudy C onduit A rtery F unction E valuation
DIABETES–RELEVANT FEATURES OF ANTIHYPERTENSIVE CLASSES ( I ) Diuretics Drug class Metabolic control Other characteristics
Worsening of dyslipidemia
Worsening of glucose tolerance
Hypokalemia
Impotence
– blockers
Worsening of dyslipidemia
Worsening of insulin resistance
Impairment of Insulin secretion
Masking of hypoglycemic symptoms
Lethargy and tiredness
Home et al , 1997
DIABETES–RELEVANT FEATURES OF ANTIHYPERTENSIVE CLASSES ( II ) Drug class Metabolic control Other characteristics
ACE inhibitors
Probably neutral
Reduced progression of nephropathy
Risk of renal deterioration
Reversible cough
Selective – blockers
Improved lipid profile
Improved insulin sensitivity
Improved sexual function
Calcium channel blockers
Netural
Peripheral edema
Increased mortality (Short acting)
Home et al , 1997
EFFECT OF ANTIHYPERTENSIVE DRUGS ON INSULIN SENSITIVITY INDEX Lithell, 1991 % Hyperinsulinemic-euglycemic clamp method
No TGL HDL Anti Oxide α β γ Adiponectin
Why should 1 blockers improve insulin sensitivity? 1 blockade: Anti-lipolytic (inhibits peripheral lipolysis) Stimulates lipoprotein lipase-mediated clearance of TGs in release of non-esterified (free) fatty acids improves muscle blood flow capillary recruitment ( LPL receptors) Prolongs transit time for blood over muscle bed in insulin hypersecretion: in hyperinsulinemia mobilization of intracellular calcium (insulin secretagogue) counter-insulin hormones CRF, cortisol, catecholamines glycogenolysis and gluconeogenesis in hyperglycemia Andersson PE . Am J Hypertens 1996; 9: 323-333.
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