Co-morbidity (HFrEF and HFpEF): hypertension

2019 ◽  
Author(s):  
Francesco Paneni ◽  
Massimo Volpe
Keyword(s):  
Blood Pressure ◽  
Ejection Fraction ◽  
Hypertensive Heart Disease ◽  
Left Ventricular ◽  
Ventricular Dilation ◽  
Hypertensive Patients ◽  
Concentric Hypertrophy ◽  
Left Ventricular Dilation ◽  
Neprilysin Inhibitor ◽  
Co Morbidity

Hypertensive heart disease is a major cause of heart failure (HF) and mortality. Hypertension precedes HF occurrence in 75% of cases, and carries a sixfold increase in HF risk as compared to non-hypertensive individuals. Most importantly, a minority of patients survive 5 years after the onset of hypertensive HF. In hypertensive patients, the heart may present different patterns of adaptive remodelling: concentric remodelling, concentric hypertrophy, and eccentric hypertrophy. Although most hypertensive patients are at high risk of developing concentric hypertrophy, a growing proportion of subjects display a concentric-to-eccentric progression eventually leading to left ventricular dilation and systolic dysfunction. Several factors including myocardial ischaemia, ethnicity, genetic background, history of diabetes, and blood pressure pattern may significantly influence the pathway from hypertension to left ventricular dilation. Patients with a concentric hypertrophy usually develop HF with preserved ejection fraction (HFpEF), whereas those with an eccentric (dilated) phenotype develop HF with reduced ejection fraction (HFrEF). Lowering blood pressure has a striking effect in reducing the risk of HF. Although available antihypertensive drugs are all successful in lowering blood pressure, angiotensin-converting enzyme inhibitors, angiotensin receptor blocker (ARBs), and diuretics are more effective than other drug classes in preventing HF. The combination of the neprilysin inhibitor sacubitril with the ARB valsartan (LCZ696) has recently been shown to be highly effective in reducing HF-related outcomes in hypertensive subjects. An individualized treatment scheme taking into account blood pressure levels, type of HF (HFpEF or HFrEF), and relevant co-morbidities (i.e. renal disease, diabetes) is currently the best approach to improve morbidity and mortality in hypertensive patients with HF.

Co-morbidity (HFrEF and HFpEF): hypertension

ESC CardioMed ◽  
2018 ◽  
pp. 1808-1812
Author(s):  
Francesco Paneni ◽  
Massimo Volpe
Keyword(s):  
Blood Pressure ◽  
Ejection Fraction ◽  
Left Ventricular ◽  
Ventricular Dilation ◽  
Hypertensive Patients ◽  
Reduced Ejection Fraction ◽  
Concentric Hypertrophy ◽  
Drug Classes ◽  
Left Ventricular Dilation ◽  
Eccentric Hypertrophy

Hypertensive heart disease is a major cause of heart failure (HF) and mortality. Hypertension precedes HF occurrence in 75% of cases, and carries a sixfold increase in HF risk as compared to non-hypertensive individuals. Most importantly, a minority of patients survive 5 years after the onset of hypertensive HF. In hypertensive patients, the heart may present different patterns of adaptive remodelling: concentric remodelling, concentric hypertrophy, and eccentric hypertrophy. Although most hypertensive patients are at high risk of developing concentric hypertrophy, a growing proportion of subjects display a concentric-to-eccentric progression eventually leading to left ventricular dilation and systolic dysfunction. Several factors including myocardial ischaemia, ethnicity, genetic background, history of diabetes, and blood pressure pattern may significantly influence the pathway from hypertension to left ventricular dilation. Patients with a concentric hypertrophy usually develop HF with preserved ejection fraction (HFpEF), whereas those with an eccentric (dilated) phenotype develop HF with reduced ejection fraction (HFrEF). Lowering blood pressure has a striking effect in reducing the risk of HF. Although available antihypertensive drugs are all successful in lowering blood pressure, angiotensin-converting enzyme inhibitors, angiotensin receptor blocker (ARBs), and diuretics are more effective than other drug classes in preventing HF. The combination of the neprilysin inhibitor sacubitril with the ARB valsartan (LCZ696) has recently been shown to be highly effective in reducing HF-related outcomes in hypertensive subjects. An individualized treatment scheme taking into account blood pressure levels, type of HF (HFpEF or HFrEF), and relevant co-morbidities (i.e. renal disease, diabetes) is currently the best approach to improve morbidity and mortality in hypertensive patients with HF.

Co-morbidity (HFrEF and HFpEF): hypertension

ESC CardioMed ◽  
2018 ◽  
pp. 1808-1812
Author(s):  
Francesco Paneni ◽  
Massimo Volpe
Keyword(s):  
Blood Pressure ◽  
Ejection Fraction ◽  
Left Ventricular ◽  
Ventricular Dilation ◽  
Hypertensive Patients ◽  
Reduced Ejection Fraction ◽  
Concentric Hypertrophy ◽  
Drug Classes ◽  
Left Ventricular Dilation ◽  
Eccentric Hypertrophy

Hypertensive heart disease is a major cause of heart failure (HF) and mortality. Hypertension precedes HF occurrence in 75% of cases, and carries a sixfold increase in HF risk as compared to non-hypertensive individuals. Most importantly, a minority of patients survive 5 years after the onset of hypertensive HF. In hypertensive patients, the heart may present different patterns of adaptive remodelling: concentric remodelling, concentric hypertrophy, and eccentric hypertrophy. Although most hypertensive patients are at high risk of developing concentric hypertrophy, a growing proportion of subjects display a concentric-to-eccentric progression eventually leading to left ventricular dilation and systolic dysfunction. Several factors including myocardial ischaemia, ethnicity, genetic background, history of diabetes, and blood pressure pattern may significantly influence the pathway from hypertension to left ventricular dilation. Patients with a concentric hypertrophy usually develop HF with preserved ejection fraction (HFpEF), whereas those with an eccentric (dilated) phenotype develop HF with reduced ejection fraction (HFrEF). Lowering blood pressure has a striking effect in reducing the risk of HF. Although available antihypertensive drugs are all successful in lowering blood pressure, angiotensin-converting enzyme inhibitors, angiotensin receptor blocker (ARBs), and diuretics are more effective than other drug classes in preventing HF. The combination of the neprilysin inhibitor sacubitril with the ARB valsartan (LCZ696) has recently been shown to be highly effective in reducing HF-related outcomes in hypertensive subjects. An individualized treatment scheme taking into account blood pressure levels, type of HF (HFpEF or HFrEF), and relevant co-morbidities (i.e. renal disease, diabetes) is currently the best approach to improve morbidity and mortality in hypertensive patients with HF.

P3835Improvement of myocardial energetic efficiency during treatment in hypertensive patients: the life study

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M A Losi ◽  
C Mancusi ◽  
E Gerdts ◽  
K Wachtell ◽  
S E Kjeldsen ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Ejection Fraction ◽  
Stroke Volume ◽  
Left Ventricular ◽  
Energetic Efficiency ◽  
Stroke Work ◽  
Hypertensive Patients ◽  
Life Study ◽  
Over Time

Abstract Background Myocardial energetic efficiency (MEE) per unit of left ventricular (LV) mass significantly predicts composite of cardiovascular (CV) events in treated hypertensive patients and specifically heart failure in an event-free population-based cohort with normal ejection fraction, independently of LV hypertrophy (LVH). Purpose To investigate whether MEEi changes over time in treated hypertensive patients, and whether different treatments have different effects. Methods From the Losartan Intervention For Endpoint study (LIFE Echo Sub-study) we selected 744 hypertensive patients (age 66±7 years; 45% women) with LVH at ECG, without atrial fibrillation, previous or incident myocardial infarction and with normal echocardiographic ejection fraction (>50%). MEE was estimated as the ratio of stroke work to the “double” product of heart rate times systolic blood pressure (BP), simplified as the ratio of stroke volume to heart rate, as previously reported. MEE was normalized for LVM (MEEi) and analyzed in quartiles at baseline and at the end treatment, according to an “intention-to-treat” protocol. Results Age and proportion of women were not significantly different from the highest to the lowest quartiles (from 65±7 to 66±7 years, p for trend=0.352; from 45% to 42%, p=0.946, respectively), whereas diastolic blood pressure (from 97±8 to 100±9 mmHg, p=0.006), prevalence of obesity (from 14 to 31%, p=0.001) and diabetes (from 4 to 14%, 0.004) progressively increased. Prevalence of concentric LV geometry and echocardiographic LVH also progressively increased from the highest to the lowest quartile (from 14 to 70%, and 61 to 90%, both p<0.0001). MEEi increased over time (p<0.007), independently of initial diastolic BP, diabetes and obesity, significantly more in patients treated with atenolol than with losartan (p<0.0001) (Figure), due to both increased stroke volume and decreased heart rate (both p<0.0001). Figure 1 Conclusions In a randomized clinical study, MEEi improves with anti-hypertensive therapy. Improvement is more evident in patients with atenolol than with losartan-based treatment, possibly providing pathophysiologic explanation of the comparable performance in prevention of ischemic heart disease previously reported in the LIFE study.

scholarly journals Impact of Diabetes on Cardiac Function in Patients with High Blood Pressure

2021 ◽  
Vol 18 (12) ◽  
pp. 6553
Author(s):  
Nabila Soufi Taleb Bendiab ◽  
Souhila Ouabdesselam ◽  
Latefa Henaoui ◽  
Marilucy Lopez-Sublet ◽  
Jean-Jacques Monsuez ◽  
...  
Keyword(s):  
Blood Pressure ◽  
High Blood Pressure ◽  
Global Longitudinal Strain ◽  
Left Ventricular ◽  
Left Ventricular Geometry ◽  
Lv Function ◽  
Hypertensive Patients ◽  
Concentric Hypertrophy ◽  
Lv Dysfunction ◽  
The Impact

Background: Although the combination of high blood pressure (HBP) and type 2 diabetes (T2DM) increases the risk of left ventricular (LV) dysfunction, the impact of T2DM on LV geometry and subclinical dysfunction in hypertensive patients and normal ejection fraction (EF) has been infrequently evaluated. Methods: Hypertensive patients with or without T2DM underwent cardiac echocardiography coupled with LV global longitudinal strain (GLS) assessment. Results: Among 200 patients with HBP (mean age 61.7 ± 9.7 years) and EF > 55%, 93 had associated T2DM. Patients with T2DM had a higher body mass index (29.9 ± 5.1 kg/m2 vs. 29.3 ± 4.7 kg/m2, p = 0.025), higher BP levels (158 ± 23/95 ± 13 vs. 142 ± 33/87 ± 12 mmHg, p = 0.003), a higher LV mass index (115.8 ± 32.4 vs. 112.0 ± 24.7 g/m2, p = 0.004), and higher relative wall thickness (0.51 ± 0.16 vs. 0.46 ± 0.12, p = 0.0001). They had more frequently concentric remodeling (20.4% vs. 16.8%, p < 0.001), concentric hypertrophy (53.7% vs. 48.6%, p < 0.001), elevated filling pressures (25.8 vs. 12.1%, p = 0.0001), indexed left atrial volumes greater than 28 mL/m2 (17.2 vs. 11.2%, p = 0.001), and a reduced GLS less than −18% (74.2 vs. 47.7%, p < 0.0001). After adjustment for BP and BMI, T2DM remains an independent determinant factor for GLS decline (OR = 2.26, 95% CI 1.11–4.61, p = 0.023). Conclusions: Left ventricular geometry and subclinical LV function as assessed with GLS are more impaired in hypertensive patients with than without T2DM. Preventive approaches to control BMI and risk of T2DM in hypertensive patients should be emphasized.

scholarly journals Ventricular-arterial coupling in hypertensive patients after TAVR. It is not all about the valve

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
F Islas ◽  
R Bottino ◽  
P Jimenez ◽  
L Nombela ◽  
P Marcos Alberca ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Left Ventricular Ejection Fraction ◽  
Aortic Stenosis ◽  
Ejection Fraction ◽  
Severe Aortic Stenosis ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Hypertensive Patients

Abstract Background In severe aortic stenosis, the left ventricle faces the challenge of the valvular load and the arterial load caused by abnormalities in systemic arterial compliance and systemic vascular resistance. The aim of this study is to assess the effect of hypertension control on left ventricular performance in patients that underwent TAVR. Methods 68 consecutive patients who underwent TAVR were analyzed; all patients were evaluated to confirm severe aortic stenosis with transthoracic echo (TTE). Conventional echo parameters were assessed as well as left ventricular mechanics parameters and vascular parameters such as arterial elastance (Ea), ventricular elastance (Ees) and V/Ac; besides all patients underwent TTE prior to TAVR, at discharge and 90 days follow-up visit. Results Mean age was 82±5; mean aortic valve area was 0.69±0.19, mean left ventricular ejection fraction was 58.3±12.1 and mean ventricular-arterial coupling was 1.6±0.9. At 90 days follow up we observed a significant worsening in V/Ac in those patients with poor control of blood pressure (&gt;140/90mmHg), (1.8±0.5 vs 2.1±0.3, p=0.03). Aortic impedance was significantly higher (4.4±1.4 vs 3.5±1.2, p=0.05); Ea and Ees were also significantly higher in hypertensive patients (2.3±0.8 vs 1.7±0.6, p=0.05) and (1.4±0.7 vs 0.9±0.6, p=0.01) respectively. Left ventricular ejection fraction (LVEF) and global longitudinal strain (GLS) showed a slightly reduction in hypertensive patients, although not statistically significant. Conclusions Control of blood pressure seems to be an important factor that contributes to a better or rather worse LV performance and could have a potential role in systolic function and clinical outcome of patients after TAVR. FUNDunding Acknowledgement Type of funding sources: None.

scholarly journals P658 Impact of hyperuricemia on left ventricular longitudinal systolic function in uncomplicated hypertensive patients

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
M Lembo ◽  
V Fazio ◽  
V Capone ◽  
L Esposito ◽  
R Sorrentino ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Uric Acid ◽  
Heart Disease ◽  
Ejection Fraction ◽  
Systolic Function ◽  
Left Ventricular ◽  
Hypertensive Patients ◽  
Fasting Glycaemia ◽  
Lv Systolic Function

Abstract Background Hyperuricemia has been reported to accelerate the occurrence and worsening of cardiovascular disease, being a risk factor for coronary heart disease and cardiac mortality. Elevated uric acid (UA) is also associated with left ventricular (LV) hypertrophy and with LV diastolic dysfunction. The effect of hyperuricemia (HU) on LV systolic function is still unclear. Purpose Aim of our study was to evaluate the impact of elevated UA serum levels on LV systolic function, also evaluating longitudinal deformation, in a population of hypertensive patients. Methods We enrolled 160 treated hypertensive patients (M/F = 104/56, age 58.2 ± 13.3 years, blood pressure = 136.7 ± 16.8/81.3 ± 10.9 mmHg), who underwent standard echo-Doppler exam, including speckle tracking quantification of global longitudinal strain (GLS, considered in absolute value). HU was defined as UA≥7 mg/dL and the study population was divided in two groups: patients with (n = 63) and without (n = 97) HU. Exclusion criteria were coronary artery disease, overt heart failure, hemodynamically significant valve heart disease, primary cardiomyopathies, permanent atrial fibrillation and inadequate echo imaging. Results The two groups were comparable for sex prevalence, blood pressure and heart rate. Patients with HU were older and had higher body mass index (BMI) (both p &lt; 0.0001). Prevalence of diabetes mellitus was higher in the group of patients with HU than in patients with normal UA (69% vs. 12% p &lt; 0.0001). Fasting glycaemia was higher (p &lt; 0.0001) and glomerular filtration rate (GFR) lower in HU hypertensives (both p &lt; 0.0001). LV mass index (LVMi) was higher in patients with HU (p &lt; 0.0001). Among diastolic parameters, transmitral E/A ratio (p &lt; 0.0001) was lower, whereas E/e’ ratio (p &lt; 0.0001), E velocity deceleration time and left atrial volume index (both p &lt; 0.001) were higher in HU hypertensives. GLS resulted to be lower in patients with HU (20.8 ± 1.5 vs. 22.3 ± 2.2%, p &lt; 0.0001). LV ejection fraction, despite still in normal range values, was also slightly lower in comparison with controls (60.6 ± 4.0 vs. 62.2 ± 3.9%, p &lt; 0.01). Serum UA levels resulted to be negatively correlated with GLS (r=-0.28, p &lt; 0.0001) (Figure), but not with ejection fraction. By a multiple linear regression analysis performed in the pooled hypertensive population, after adjusting for age, BMI, GFR, fasting glycaemia and LVMi, the association between UA levels and GLS remained significant (standardized beta coefficient =-0.25, p &lt; 0.01), besides the significant impact of age (beta=-0.19 , p &lt; 0.05). Conclusions In hypertensive patients with multiple cardiovascular risk factors, the presence of HU is associated with LV diastolic and systolic dysfunction. Serum UA levels and GLS resulted independently associated even after adjusting for several clinical and echo confounders. Acid uric might be considered as an independent marker of early LV dysfunction, able to identify hypertensive patients at increased risk for heart failure. Abstract P658 Figure. Relation between uric acid and GLS

scholarly journals Hypertensive heart disease: Benefit of carvedilol in hemodynamic, left ventricular remodeling, and survival

2019 ◽  
Vol 7 ◽  
pp. 205031211882358 ◽  
Author(s):  
Renata F Dominguez ◽  
Valeria A da Costa-Hong ◽  
Luan Ferretti ◽  
Fabio Fernandes ◽  
Luiz A Bortolotto ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heart Disease ◽  
Left Ventricular Ejection Fraction ◽  
Ejection Fraction ◽  
Hypertensive Heart Disease ◽  
Left Ventricular ◽  
Ventricular Ejection ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction

Objectives: The aim of this study was to determine if carvedilol improved structural and functional changes in the left ventricle and reduced mortality in patients with hypertensive heart disease. Methods: Blood pressure, heart rate, echocardiographic parameters, and laboratory variables, were assessed pre and post treatment with carvedilol in 98 eligible patients. Results: Carvedilol at a median dose of 50 mg/day during the treatment period in hypertensive heart disease lowered blood pressure 10/10 mmHg, heart rate 10 beats/min, improved left ventricular ejection fraction from baseline to follow-up (median: 6 years) (36%–47%)) and reduced left ventricular end-diastolic and end-systolic dimensions (62 vs 56 mm; 53 vs 42 mm, respectively, all p-values <0.01). Left ventricular ejection fraction increased in 69% of patients. Patients who did not have improved left ventricular ejection fraction had nearly six-fold higher mortality than those that improved (relative risk; 5.7, 95% confidence interval: 1.3–25, p = 0.022). Conclusion: Carvedilol reduced cardiac dimensions and improved left ventricular ejection fraction and cardiac remodeling in patients with hypertensive heart disease. These treatment-related changes had a favorable effect on survival.

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