Hypertensive left ventricular hypertrophy risk: beyond adaptive cardiomyocytic hypertrophy

Fröhlich, Edward D.; González, Arantxa; Díez, Javier

doi:10.1097/hjh.0b013e328340d787

Cited by 68 publications

(47 citation statements)

References 114 publications

(107 reference statements)

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“…25 Excess sodium intake in experimental animals also promotes left and right ventricular hypertrophy and fibrosis, perivascular fibrosis of the coronary arteries, and diastolic dysfunction. 24,26 These findings in animal studies are strikingly similar to those seen in patients with similarly impaired left ventricular function, the most common basis for cardiac and renal failure and hospitalization in Medicare patients. 27 Even in young healthy adults with clinically normal BP, those who consume more sodium and less potassium are more likely to have increased left ventricular mass; this is especially prominent when BP is elevated, suggesting that excess dietary sodium sensitizes the heart, large arteries, and kidneys to hypertrophic and fibrotic stimuli.…”

Section: Experimental and Clinical Laboratory Studiessupporting

confidence: 61%

“…27 Even in young healthy adults with clinically normal BP, those who consume more sodium and less potassium are more likely to have increased left ventricular mass; this is especially prominent when BP is elevated, suggesting that excess dietary sodium sensitizes the heart, large arteries, and kidneys to hypertrophic and fibrotic stimuli. 25,26 A challenge in studying the impact of excess sodium intake in humans is that target-organ damage often develops slowly, likely over many years. Moreover, these target-organ effects, especially kidney injuries, can make BP more salt sensitive over time.…”

Section: Experimental and Clinical Laboratory Studiesmentioning

confidence: 99%

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Sodium, Blood Pressure, and Cardiovascular Disease

Whelton¹,

Appel²,

Sacco³

et al. 2012

Circulation

386

138

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Abstract-Recent reports of selected observational studies and a meta-analysis have stirred controversy and have become the impetus for calls to abandon recommendations for reduced sodium intake by the US general population. A detailed review of these studies documents substantial methodological concerns that limit the usefulness of these studies in setting, much less reversing, dietary recommendations. Indeed, the evidence base supporting recommendations for reduced sodium intake in the general population remains robust and persuasive. The American Heart Association is committed to improving the health of all Americans through implementation of national goals for health promotion and disease prevention, including its recommendation to reduce dietary sodium intake to Ͻ1500 mg/d. (Circulation. 2012;126:2880-2889.)Key Words: AHA Scientific Statements Ⅲ sodium Ⅲ diet Ⅲ prevention I n almost every country that has established guidelines for the prevention and treatment of cardiovascular disease (CVD) and stroke, national health agencies and professional societies recommend a reduction in dietary sodium as a means to lower blood pressure (BP) and to prevent CVD and stroke. The American Heart Association (AHA) currently recommends a sodium intake Ͻ1500 mg/d for the entire US population. 1 The US Department of Agriculture and US Department of Health and Human Services joint 2010 Dietary Guidelines for Americans calls for no more than 1500 mg/d in AfricanAmericans, people Ͼ51 years of age, and people with hypertension, diabetes mellitus, or chronic kidney disease, and no more than 2300 mg/d in all others. 2 Guideline recommendations far exceed adequate intake for sodium in some age groups, especially in children; the adequate intake for children aged 1 to 3 years is 1000 mg/d, and for children aged 4 to 8 years is 1200 mg/d. 3 The scientific rationale for the AHA recommendation was documented in an AHA presidential advisory published in 2011. 4 The principal basis for the recommendation was the strength of the evidence relating excess sodium intake to high BP, CVD, and stroke and the capacity of reduced intake of sodium to prevent and treat hypertension and to reduce the risk of adverse CVD and stroke events. High BP, both prehypertension and hypertension, is a leading cause of preventable morbidity and mortality worldwide. 5 Excess sodium intake has also been linked to kidney stones, asthma, osteoporosis, and gastric cancer. 3,6 Various local, state, federal, and global initiatives are focused on efforts to meet sodium reduction guidelines. 7 Even a modest reduction in sodium intake is likely to result in substan-The opinions expressed in this article are not necessarily those of the editors. The American Heart Association makes every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside relationship or a personal, professional, or business interest of a member of the writing panel. Specifically, all members of the writing group are required to complete and submit a Discl...

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Section: Experimental and Clinical Laboratory Studiessupporting

confidence: 61%

Section: Experimental and Clinical Laboratory Studiesmentioning

confidence: 99%

Sodium, Blood Pressure, and Cardiovascular Disease

Whelton¹,

Appel²,

Sacco³

et al. 2012

Circulation

386

138

View full text Add to dashboard Cite

show abstract

“…8 With pathological left ventricular hypertrophy, structural remodeling takes place, resulting in reduced coronary flow reserve, among other consequences. 21 For other outcomes, a causal pathway is less obvious.…”

Section: Discussionmentioning

confidence: 99%

Association of High Ankle Brachial Index With Incident Cardiovascular Disease and Mortality in a High-Risk Population

Hendriks

Westerink

Jong

et al. 2016

ATVB

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Objective— The objective of this present study is to determine whether high ankle brachial index (ABI) as compared with ABIs within reference limits is associated with an increased incidence of cardiovascular disease (CVD) events and all-cause mortality in a high-risk population and whether this association is the same for patients with and without diabetes mellitus or prevalent CVD. Approach and Results— Seven thousand five hundred and thirty-eight patients with ABI>0.9 and either prevalent CVD or a high risk for CVD were selected from the Second Manifestations of Arterial Disease (SMART) study. Three hundred and thirty-six participants (4.5%) had high ABI (≥1.4 or incompressible). Higher age, male sex, higher body mass index, and diabetes mellitus were associated with higher prevalences of high ABI; smoking and higher non–high-density lipoprotein levels were associated with lower prevalences of high ABI. Cox proportional hazards models were fitted assessing the association of high ABI (as compared with ABI 0.9–1.4) with the risk of myocardial infarction, stroke, cardiovascular death, the combined outcome of these 3, and total mortality (median follow-up 6.9 years). After multivariable adjustment, high ABI was associated with an increased risk of myocardial infarction (hazard ratio 1.83 [95% confidence interval 1.22–2.76]), but not with stroke (hazard ratio 0.86 [95% confidence interval 0.44–1.69]), cardiovascular (hazard ratio 1.14 [95% confidence interval 0.70–1.84]), or all-cause mortality (hazard ratio 0.95 [95% confidence interval 0.67–1.34]). Associations of high ABI with CVD outcomes tended to be stronger in patients with diabetes mellitus but without statistically significant interactions. Conclusions— In a high-risk population, the presence of an ABI≥1.4 was associated with an increased risk for myocardial infarction, but not with stroke, all-cause, or vascular mortality.

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“…Frohlich et al (20) have concluded that contrary to the physiological LV hypertrophy, pathological LV hypertrophy is accompanied by a poor prognosis.…”

Section: Diagnosis Of Left Ventricular Hypertrophymentioning

confidence: 99%

“…The balance between mitochondria and contractile elements, called mitochondrial/myofibril volume ratio, is of prime importance. An imbalance of this ratio may lead to disturbance of energy supply of the myocytes (19,20).…”

Section: Pathophysiology Of Left Ventricular Hypertrophymentioning

confidence: 99%

How to estimate left ventricular hypertrophy in hypertensive patients

Lović¹,

Erdine²,

Çatakoğlu³

2014

Anadolu Kardiyol Derg

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Left ventricular hypertrophy (LVH) is a structural remodeling of the heart developing as a response to volume and/or pressure overload. Previous studies have shown that hypertension is not an independent factor in the development of LVH and occurrence does not depend on the length and severity of hypertension, but the role played by other comorbidities such as triglycerides, age, gender, genetics, insulin resistance, obesity, physical inactivity, increased salt intake and chronic stress. LVH develops through three phases: adaptive, compensatory, and pathological phase. Contractile dysfunction is reversible in the first two phases and irreversible in the third. According to the Framingham study, LVH develops in 15-20% of patients with mild arterial hypertension, and in 50% of patients with severe hypertension. The pathophysiology of LVH includes hypertrophy of cardiomyocytes, interstitial and perivascular fibrosis, coronary microangiopathy and macroangiopathy. Individuals with LVH have 2-4 times higher risk of having adverse CV events compared to patients without LVH. (Anadolu Kardiyol Derg 2014; 14: 389-95)

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Hypertensive left ventricular hypertrophy risk: beyond adaptive cardiomyocytic hypertrophy

Cited by 68 publications

References 114 publications

Sodium, Blood Pressure, and Cardiovascular Disease

Sodium, Blood Pressure, and Cardiovascular Disease

Association of High Ankle Brachial Index With Incident Cardiovascular Disease and Mortality in a High-Risk Population

How to estimate left ventricular hypertrophy in hypertensive patients

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