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Results for “Hypertrophy, Left Ventricular”

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PubMed1993

Left ventricular diastolic dysfunction late after coarctation repair in childhood: influence of left ventricular hypertrophy.

OBJECTIVES: Left ventricular systolic and diastolic function were evaluated late after successful operation for aortic coarctation in childhood. BACKGROUND: Persistent arterial hypertension and left ventricular hypertrophy after coarctation repair might impair left ventricular function. METHODS: Biplane angiography and simultaneous high fidelity pressure measurements were performed in 12 patients 3 to 12 years postoperatively (residual pressure gradient 4 mm Hg). Eight patients were normotensive and four had borderline hypertension. Data at rest and after nitroprusside infusion (1.7 micrograms/kg per min) were evaluated and compared with data from 12 control subjects. RESULTS: Systolic left ventricular function (ejection fraction-end-systolic wall stress relation) was normal in all patients. However, left ventricular muscle mass (113 vs. 86 g/m2), right atrial pressure (5.2 vs. 1.9 mm Hg) and left ventricular end-diastolic pressure (16 vs. 11 mm Hg) were significantly higher in patients than in control subjects. There was a linear relation between muscle mass and left ventricular end-diastolic (r = 0.66, p < 0.001) or right atrial (r = 0.60, p < 0.01) pressure. Left ventricular relaxation and myocardial stiffness were normal. However, there was an upward shift of the diastolic pressure-volume curve when compared with control values, but this shift was reversed by the administration of nitroprusside. CONCLUSIONS: Systolic function is normal late after coarctation repair. However, diastolic function can be abnormal with an upward shift of the diastolic pressure-volume curve that is reversed by nitroprusside administration and is probably due to residual left ventricular hypertrophy.

Adolescent↗

PubMed1990

Iodine-123 phenylpentadecanoic acid myocardial scintigraphy in patients with left ventricular hypertrophy: alterations in left ventricular distribution and utilization.

Regional alterations in myocardial substrate uptake and/or utilization have been demonstrated in rats with hypertension. To determine whether alterations in left ventricular fatty acid uptake and/or utilization are present in patients with left ventricular hypertrophy (LVH), we compared the results of rest and exercise iodine-123 phenylpentadecanoic acid (IPPA) myocardial scintigraphy in 10 patients with hypertension who had concentric LVH without evidence of coronary artery disease and in 15 normal subjects. Patients with LVH had more heterogeneous left ventricular activity of IPPA compared to normal subjects after exercise but not at rest (23 +/- 8% versus 13 +/- 5% difference in maximum segmental activity at 4 minutes after exercise; p = 0.005). Although IPPA clearance was similar in both patients with LVH and normal subjects, postexercise washout in segments showing decreased initial IPPA uptake was reduced compared to washout at rest in patients with LVH (11.7 +/- 7.5% versus 21.5 +/- 8.4% at 20 minutes after injection, n = 15; p = 0.005). Exercise thallium-201 (TI-201) scintigraphy was normal in all seven patients with LVH tested. Patients with LVH showed significantly greater heterogeneity in IPPA uptake compared to TI-201 uptake immediately after exercise (25 +/- 5% versus 16 +/- 6%; p = 0.013). We conclude that (1) compared to normal subjects, patients with LVH show heterogeneous myocardial IPPA activity after exercise but not at rest; (2) postexercise washout of IPPA was decreased in segments with reduced uptake after exercise in patients with LVH; and (3) the distribution of IPPA is more heterogeneous than that of TI-201 immediately after exercise in patients with concentric LVH. The postexercise heterogeneity in IPPA uptake and delayed washout in segments with reduced initial uptake is consistent with exercise-induced myocardial ischemia in patients with LVH.

Adult↗

PubMed1997

[Studies on residual cardiovascular dysfunction in patients receiving long-term antihypertensive treatment of calcium channel blockers: with special reference to left ventricular hypertrophy, and impairments of left ventricular diastolic function and carotid arterial distensibility].

Residual cardiovascular dysfunctions including left ventricular hypertrophy, and impairment of left ventricular diastolic function and carotid arterial distensibility were investigated in hypertensive patients treated with calcium channel blockers for more than 1 year. Ultrasonographic examinations of the heart and carotid artery were performed in patients treated with calcium channel blocker alone for more than 1 year (n = 45) and in age-, sex- and weight-matched control subjects (n = 29). The following parameters were obtained: left ventricular mass index, cardiac diastolic function (A/E ratio) and carotid arterial distensibility (Distens). Hypertensive subjects were re-examined under the same conditions with the same parameters after 10 +/- 5 months. Patients with hypertension revealed no significant changes in these three parameters after 10 +/- 5 months Patients with left ventricular hypertrophy (n = 20) revealed significant impairments in diastolic function and carotid arterial distensibility (A/E = 1.42 +/- 0.25, Distens = 2.4 +/- 1.3% kPa) compared to those without left ventricular hypertrophy (n = 25) (A/E = 1.18 +/- 0.29, Distens = 3.8 +/- 1.7% kPa, p < 0.05). Patients without left ventricular hypertrophy had significantly impaired cardiovascular functions compared to the normal control group (A/E = 1.03 +/- 0.27, Distens = 6.3 +/- 2.2% kPa, p < 0.05, p < 0.01 respectively). Therefore, only reduction of blood pressure with calcium channel blocker may not be enough to improve cardiovascular organ damage, especially in patients with residual left ventricular hypertrophy, and such residual functional deteriorations must be corrected probably with another pharmaceutical modality.

Aged↗

PubMed1996

[Effects of Peucedanum praeruptorum extractum on blood pressure, left ventricular hypertrophy and hemodynamic changes in left ventricular hypertrophied hypertensive rats].

After intragastric administration of Peucedanum praeruptorum (PPE) 0.6 g/100 g body weight, the blood pressure was decreased significantly in both the normal and the left ventricular hypertrophied hypertensive (LVH) rats. The PPE could still prevent the formation of the left ventricular hypertrophy in renovascular hypertensive rats, the ratio of weight of left ventricular over the weight of body was reduced markedly than that of the LVH group, and was nearly the same of the sham-operated group. The PPE could improve both the systolic and diastolic function than that of the LVH group in the isolated heart, especially, the flow of the coronary artery was increased significantly.

Animals↗

PubMed1984

Electrocardiographic detection of left ventricular hypertrophy using echocardiographic determination of left ventricular mass as the reference standard. Comparison of standard criteria, computer diagnosis and physician interpretation.

Electrocardiographic findings of left ventricular hypertrophy were compared with echocardiographic left ventricular mass in 148 patients to assess performance of standard electrocardiographic criteria, the IBM Bonner program and physician interpretation. On echocardiography, 43% of the patients had left ventricular hypertrophy (left ventricular mass greater than 215 g). Sokolow-Lyon voltage-(S in V1 + R in V5 or V6) and Romhilt-Estes point score correlated modestly with left ventricular mass (r = 0.40, p less than 0.001 and r = 0.55, p less than 0.001, respectively). Sensitivity of Sokolow-Lyon voltage greater than 3.5 mV for left ventricular hypertrophy was only 22%, but specificity was 93%. Point score for probable left ventricular hypertrophy (greater than or equal to 4 points) had 48% sensitivity and 85% specificity, whereas definite hypertrophy (greater than or equal to 5 points) had 34% sensitivity and 98% specificity. Computer analysis resulted in 45% sensitivity and 83% specificity. Overall diagnostic accuracy of the IBM Bonner program (67%) was better than that of Sokolow-Lyon voltage (62%), but worse than the Romhilt-Estes point score (69% for greater than or equal to 4 points or 70% for greater than or equal to 5 points). Three cardiologists interpreted electrocardiograms independently and in a blinded fashion. Physician sensitivity was 56%, specificity 92% and accuracy 76%. Correlation with left ventricular hypertrophy was good (r = 0.70, p less than 0.001). It is concluded that: 1) computer diagnosis of left ventricular hypertrophy by the IBM Bonner program is no more accurate than diagnosis by Sokolow-Lyon or Romhilt-Estes criteria, and 2) physician recognition of left ventricular hypertrophy is more accurate.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1995

Hypertension and left-ventricular hypertrophy.

Left-ventricular hypertrophy (LVH), the primary cardiac manifestation of hypertension, has been identified as the most powerful risk factor for future cardiovascular events causing morbidity and mortality, such as myocardial infarction, congestive heart failure, sudden death, and so forth. The increase in myocardial mass lowers coronary reserve and enhances cardiac oxygen requirements, gives rise to ventricular ectopy, and impairs left-ventricular filling and contractility. Besides hypertension, other risk factors such as obesity, advanced age, valvular heart disease, and other pathologic disorders can cause an increase in the hemodynamic burden and lead to LVH. Nonhemodynamic determinants of left-ventricular mass include dietary salt intake, alcohol, and neurohormones. LVH and its sequelae can be reduced by specific antihypertensive therapy, but despite these promising findings, future epidemiologic studies are necessary to document the clinical benefits of a reduction in LVH.

Cardiovascular Diseases↗

PubMed2006

Gender differences in electrical remodeling and susceptibility to ventricular arrhythmias in rabbits with left ventricular hypertrophy.

BACKGROUND: Left ventricular hypertrophy (LVH) is associated with an increased risk of death, vulnerability to ventricular arrhythmia, and multiple electrophysiological abnormalities. OBJECTIVES: The purpose of the present study was to determine the gender-dependent differences in electrical remodeling and the susceptibility to ventricular arrhythmias in a rabbit model of renovascular hypertension. METHODS: Rabbits of both sexes underwent unilateral renal artery banding and contralateral nephrectomy or were placed in the control group. Data are expressed as mean +/- standard error of the mean. RESULTS: The duration of action potentials was prolonged in the LVH group compared with the control group in both male (123 +/- 2.4 ms and 151 +/- 2.3 ms vs. 180 +/- 5.1 ms and 196 +/- 3.1 ms for action potential duration [APD](90 Epi) and APD(90 Endo) of control [n = 5] and LVH rabbits [n = 8], respectively; P<.05) and female rabbits (131 +/- 1.9 ms and 166 +/- 2.0 ms vs. 156 +/- 4.2 ms and 175 +/- 2.2 ms for APD(90 Epi) and APD(90 Endo) of control [n = 5] and LVH rabbits [n = 7], respectively; P<.05). Moreover, the gender-dependent differences in repolarization were opposite to those seen under control conditions. In LVH rabbits, APD(90) was greater in males than in females. The changes induced in APD lead to a greater transmural dispersion of repolarization (38 +/- 6.6 ms vs. 19 +/- 6.5 ms for males and females, respectively; P<.05). In addition, while control rabbits did not show induction of arrhythmias, an enhanced susceptibility to ventricular arrhythmia was seen in LVH male rabbits (6/8 male vs. 1/7 female LVH rabbits; P<.05). CONCLUSION: We conclude that the electrical remodeling associated with LVH inverted the gender-dependent differences, with male rabbits now exhibiting action potentials with longer durations both in the endocardial and epicardial surface of the left ventricle, increased dispersion of repolarization, and increased vulnerability to ventricular arrhythmia induction.

Action Potentials↗

PubMed1994

Induction of myocardial insulin-like growth factor-I gene expression in left ventricular hypertrophy.

BACKGROUND: Left ventricular hypertrophy is a generalized adaptation to increased afterload, but the growth factors mediating this response have not been identified. To explore whether the hypertrophic response was associated with changes in local insulin-like growth factor-I (IGF-I) gene regulation, we examined the induction of the cardiac IGF-I gene in three models of systolic hypertension and resultant hypertrophy. METHODS AND RESULTS: The model systems were suprarenal aortic constriction, uninephrectomized spontaneously hypertensive rats (SHR), and uninephrectomized, deoxycorticosterone-treated, saline-fed rats (DOCA salt). Systolic blood pressure reached hypertensive levels at 3 to 4 weeks in all three systems. A differential increase in ventricular weight to body weight (hypertrophy) occurred at 3 weeks in the SHR and aortic constriction models and at 4 weeks in the DOCA salt model. Ventricular IGF-I mRNA was detected by solution hybridization/RNase protection assay. IGF-I mRNA levels increased in all three systems coincident with the onset of hypertension and the development of ventricular hypertrophy. Maximum induction was 10-fold over control at 5 weeks in the aortic constriction model, 8-fold at 3 weeks in the SHR, and 6-fold at 6 weeks in the DOCA salt model. IGF-I mRNA levels returned to control values by the end of the experimental period despite continued hypertension and hypertrophy in all three systems. In contrast, ventricular c-myc mRNA content increased twofold to threefold at 1 week and returned to control levels by 2 weeks. Ventricular IGF-I receptor mRNA levels were unchanged over the time course studied. The increased ventricular IGF-I mRNA content was reflected in an increased ventricular IGF-I protein content, as determined both by radioimmunoassay and immunofluorescence histochemistry. CONCLUSIONS: We conclude that (1) hypertension induces significant increases in cardiac IGF-I mRNA and protein that occur coordinately with its onset and early in the development of hypertrophy, (2) IGF-I mRNA levels normalize as the hypertrophic response is established, (3) in comparison to IGF-I, both c-myc and IGF-I receptor genes are differentially controlled in experimental hypertension. These findings suggest that IGF-I may participate in initiating ventricular hypertrophy in response to altered loading conditions. The consistency of these findings in models of high-, moderate-, and low-renin hypertension suggests that they occur independently of the systemic renin-angiotensin endocrine axis.

Animals↗

PubMed2006

Comparison of the protein profile of established and regressed hypertension-induced left ventricular hypertrophy.

Established left ventricular hypertrophy (LVH) showed a significant alteration in the cardiac protein profile compared with normal heart. The main finding of this work was to identify proteins differently expressed in hypertension-induced LVH and the fact that after regression of LVH (histologically determined), the proteome still maintains a number of expressed proteins characteristic of the hypertrophied heart. These unrecovered proteins play an essential role in the energy production pathway, in cellular stress defense and also in hypertrophy regulation.

Amino Acid Sequence↗

PubMed2006

Estrogen receptor beta protects the murine heart against left ventricular hypertrophy.

BACKGROUND: Left ventricular hypertrophy (LVH) displays significant gender-based differences. 17beta-estradiol (E2) plays an important role in this process because it can attenuate pressure overload hypertrophy via 2 distinct estrogen receptors (ERs): ERalpha and ERbeta. However, which ER is critically involved in the modulation of LVH is poorly understood. We therefore used ERalpha-deficient (ERalpha-/-) and ERbeta-deficient (ERbeta-/-) mice to analyze the respective ER-mediated effects. METHODS AND RESULTS: Respective ER-deficient female mice were ovariectomized and were given E2 or placebo subcutaneously using 60-day release pellets. After 2 weeks, they underwent transverse aortic constriction (TAC) or sham operation. In ERalpha-/- animals, TAC led to a significant increase in ventricular mass compared with sham operation. E2 treatment reduced TAC induced cardiac hypertrophy significantly in wild-type (WT) and ERalpha-/- mice but not in ERbeta-/- mice. Biochemical analysis showed that E2 blocked the increased phosphorylation of p38-mitogen-activated protein kinase observed in TAC-treated ERalpha-/- mice. Moreover, E2 led to an increase of ventricular atrial natriuretic factor expression in WT and ERalpha-/- mice. CONCLUSIONS: These findings demonstrate that E2, through ERbeta-mediated mechanisms, protects the murine heart against LVH.

Animals↗

PubMed2002

Endogenous nitric oxide prevents myocardial ischemia in patients with hypertension and left ventricular hypertrophy.

BACKGROUND: Left ventricular hypertrophy (LVH) caused by chronic pressure overload is associated with increased risk of myocardial ischemia without epicardial coronary artery disease. We aimed to test the hypothesis that endogenous nitric oxide (NO) prevents myocardial ischemia in patients with LVH. METHODS: Epicardial coronary blood flow (Doppler wire and quantitative coronary arteriography) and myocardial lactate metabolism (paired arterial and coronary sinus blood sampling) were measured in 12 patients with hypertension, LVH, and angiographically normal epicardial coronary arteries and in 7 control subjects. Measurements were done under 3 pacing protocols: with no treatment (control), with intracoronary N(G)-monomethyl-L-arginine (L-NMMA; NO synthesis inhibitor), and with intracoronary L-arginine (NO substrate). RESULTS: In control subjects the myocardial lactate extraction ratio was normal and stable during the 3 pacing protocols. In contrast, lactate uptake was significantly decreased from 0.21 +/- 0.05 to 0.10 +/- 0.06 (P <.05) during L-NMMA pacing in patients with LVH; in 6 of them, lactate production was demonstrated. After L-arginine administration, the lactate extraction ratio during pacing was normalized (0.18 +/- 0.04) and lactate production was not observed in any patient. The level of myocardial lactate uptake at peak pacing after L-NMMA was correlated with that under untreated condition (P <.0001). CONCLUSIONS: In patients with hypertension, LVH, and angiographically normal coronary arteries, inhibition of endogenous NO synthesis in the coronary circulation unmasked myocardial ischemia during tachycardia, and L-arginine reversed the adverse effects of L-NMMA. Although the precise mechanism remains to be determined, our results suggest that constitutive NO in the coronary circulation plays an anti-ischemic role in this population.

Aged↗

PubMed2006

Attenuated cardioprotective response to bradykinin, but not classical ischaemic preconditioning, in DOCA-salt hypertensive left ventricular hypertrophy.

Hypertensive left ventricular hypertrophy (LVH) co-exists frequently with ischaemic heart disease. While ischaemic preconditioning (IPC) is known to protect against ischaemia-reperfusion injury in LVH, it is not known if other cardioprotective manoeuvres are effective. Bradykinin, a key autacoid mediator in IPC, is protective in normal hearts but its ability to protect against ischaemia-reperfusion injury in LVH is unknown. Hypertensive LVH was induced in male rats by 4 weeks treatment with deoxycorticosterone acetate (DOCA) and salt drinking fluid. Hearts were Langendorff perfused, subjected to 35 min coronary artery occlusion and 120 min reperfusion, and infarct size (AN/RZ %) was determined by tetrazolium staining. The effects of IPC with 2 x 5 min cycles of global ischaemia or 10 min pretreatment with bradykinin were assessed. DOCA-salt rats were markedly hypertensive and left ventricle/body weight ratio was 26% greater than in normotensive controls. Baseline coronary flow and risk zone/LV ratio were similar in normotensive hearts and DOCA-salt hearts, and infarct size was similar (AN/RZ 50.6+/-3.2% and 47.0+/-3.1%, respectively). IPC was equally protective in normotensive and DOCA-salt hearts (AN/RZ 18.6+/-3.3% and 18.4+/-2.3%, respectively, P < 0.01 versus corresponding control). Bradykinin 0.1, 0.2 or 0.5 microM pretreatment produced concentration-dependent infarct limitation in normotensive hearts (bradykinin 0.5 microM AN/RZ, 9.5+/-3.6%, P < 0.01 versus normotensive control), but the effect in DOCA-salt hearts was attenuated (bradykinin 0.5 microM AN/RZ, 23.4+/-3.8%). Further, the pre-ischaemic coronary vasodilator response to bradykinin was abrogated in DOCA-salt hypertensive hearts. We conclude that the cardioprotective action of bradykinin is markedly attenuated in moderate LVH and coronary vasodilator effect is lost. The reasons for reduced sensitivity to bradykinin in the hypertensive heart are unknown but these findings may have implications for the application of preconditioning-mimetic interventions in LVH.

Animals↗

PubMed2000

New quantitative methods of ventricular repolarization analysis in patients with left ventricular hypertrophy.

BACKGROUND: Left ventricular hypertrophy (LVH) is accompanied by specific changes in ventricular electrophysiology, which are potentially arrhythmogenic. Nevertheless, the electrocardiographic diagnostic signs for LVH have a relatively low predictive power for arrhythmic events and sudden death. We thought that other parameters derived from the surface ECG, not apparent at visual inspection, might be detected by specific analysis of electrocardiographic digital recordings. The purpose of our work was to analyze the surface distribution of repolarization potentials and search for subtle alterations not revealed by the usual electrocardiographic processing, which are likely to reflect ventricular repolarization heterogeneity. METHODS: Body surface potential maps were recorded from 62 chest leads in 16 patients with LVH due to aortic stenosis and in 35 normal subjects. By applying a principal component analysis of the ST-T waves, we computed the similarity index. The value of the similarity index is inversely proportional to the variability of T wave morphology and a low value is considered a marker of repolarization heterogeneity. RESULTS: The similarity index was significantly lower in LVH patients than in normals both in 62 leads (0.73 +/- 0.067 vs 0.77 +/- 0.044, p = 0.03) and in 12 unipolar leads (V1- V8, V3R, VR, VL, VF) extracted from the map (0.77 +/- 0.075 vs 0.81 +/- 0.045, p = 0.03). Moreover, we computed the "late repolarization deviation index", which quantifies the instantaneous variations of surface potential distribution from peak to end of the T wave. This index was significantly higher in LVH patients than in controls (in 62 leads 0.07 +/- 0.05 vs 0.028 +/- 0.016, p = 0.005; in 12 leads 0.064 +/- 0.052 vs 0.024 +/- 0.020, p = 0.008). CONCLUSIONS: The values of similarity index and of late repolarization deviation index found in LVH patients suggest a higher than normal degree of repolarization heterogeneity, not detected by the usual electrocardiographic analysis. Since both indices maintained statistical significance when calculated on the 12 leads derived from our map lead system, they could be reliably computed from digital recordings of the 12 conventional leads.

Adult↗

PubMed2004

Serum carboxyl-terminal propeptide of procollagen type I in exercise-induced left ventricular hypertrophy.

BACKGROUND: Left ventricular hypertrophy (LVH) induced by exercise is considered to be a physiologic adaptive mechanism without fibrogenic hyperactivity, as occurs in pathologic hypertrophy. HYPOTHESIS: This study investigated serum markers of collagen synthesis and echo parameters of left ventricular diastolic function (LVdf) in 22 male athletes. METHODS: Twenty-two highly competitive male athletes (10 cyclists, 12 soccer players) were studied with full history, clinical examination, Doppler echocardiogram, and serum concentration of the carboxyl-terminal propeptide of collagen type I (PIP). They were divided into two groups: normal left ventricular mass (N) with left ventricular mass index (LVMI) < 125 g/m2 (14 athletes) and LVH with LVMI > 125 g/m2 (8 athletes). RESULTS: Age, body surface area, blood pressure, heart rate, and systolic function were not different between the groups. Serum concentration of PIP (N: 163 +/- 44.1 microg/l, LVH: 172.7 +/- 61.2 microg/l--NS) and LVdf (early to atrial peak mitral flow velocity ratio: [E/A] N: 1.77 +/- 0.47, LVH: 1.98 +/- 0.70--NS, and early to atrial peak mitral annulus velocity ratio: [Ea/Aa] N: 2.63 +/- 0.70, LVMI: 2.55 +/- 0.90 LV 1.61--NS) were similar in both groups. CONCLUSIONS: Normal serum concentration of PIP in athletes with LVH in association with normal LVdf indicates the possibility that in this type of physiologic hypertrophy there is mainly an increase of myocyte size without interstitial fibrosis.

Adolescent↗

PubMed2000

Echocardiographic predictors of clinical outcome in patients with left ventricular dysfunction enrolled in the SOLVD registry and trials: significance of left ventricular hypertrophy. Studies of Left Ventricular Dysfunction.

OBJECTIVES: To assess the relation of left ventricular (LV) and left atrial (LA) dimensions, ejection fraction (EF) and LV mass to subsequent clinical outcome of patients with LV dysfunction enrolled in the Studies of Left Ventricular Dysfunction (SOLVD) Registry and Trials. BACKGROUND: Data are lacking on the relation of LV mass to prognosis in patients with LV dysfunction and on the interaction of LV mass with other measurements of LV size and function as they relate to clinical outcome. METHODS: A cohort of 1,172 patients enrolled in the SOLVD Trials (n = 577) and Registry (n = 595) had baseline echocardiographic measurements and follow-up for 1 year. RESULTS: After adjusting for age, New York Heart Association (NYHA) functional class, Trial vs. Registry and ischemic etiology, a 1-SD difference in EF was inversely associated with an increased risk of death (risk ratio, 1.62; p = 0.0008) and cardiovascular (CV) hospitalization (risk ratio, 1.59; p = 0.0001). Consequently, the other echo parameters were adjusted for EF in addition to age, NYHA functional class, Trial vs. Registry and ischemic etiology. A 1-SD difference in LV mass was associated with increased risk of death (risk ratio of 1.3, p = 0.012) and CV hospitalization (risk ratio of 1.17, p = 0.018). Similar results were observed with the LA dimension (mortality risk ratio, 1.32; p < 0.02; CV hospitalizations risk ratio, 1.18; p < 0.04). Likewise, LV mass > or =298 g and LA dimension > or =4.17 cm were associated with increased risk of death and CV hospitalization. An end-systolic dimension >5.0 cm was associated with increased mortality only. A protective effect of EF was noted in patients with LV mass > or =298 g (those in the group with EF >35% had lower mortality) but not in the group with LV mass <298 g. CONCLUSIONS: In patients with LV dysfunction enrolled in the SOLVD Registry and Trials, increasing levels of hypertrophy are associated with adverse events. A protective effect of EF was noted in patients with LV mass > or =298 g (those in the group with EF >35% fared better) but not in the group with LV mass <298 g. These data support the development and use of drugs that can inhibit hypertrophy or alter its characteristics.

Aged↗

PubMed1989

Effects of atenolol on left ventricular hypertrophy and early left ventricular function in essential hypertension.

Echocardiographic studies of left ventricular (LV) hypertrophy indicate clinical benefits of antihypertensive therapy. Therefore, M-mode and Doppler techniques were used to assess changes in LV hypertrophy after 10, 30 and 50 weeks of atenolol therapy (50 or 100 mg once daily) in 19 patients with essential hypertension. After 50 weeks of atenolol treatment, the most notable changes were: for M-mode parameters, increases (p less than 0.05) in diastolic LV internal dimension, radius to thickness ratio and stroke volume, and decreases (p less than 0.01) in total wall thickness and heart rate; for Doppler parameters, increases (p less than 0.01) in slope and peripheral resistance, and decreases (p less than 0.01) in heart rate, stroke volume and cardiac output. The decreased total wall thickness and increased radius to thickness ratio suggest a trend toward regression of LV hypertrophy. These findings, along with improvements in blood pressure, pulse and exercise stress tests, indicate potential benefits of atenolol in managing patients with essential hypertension and LV hypertrophy.

Adult↗

PubMed1995

[Effects of m-nifedipine on left ventricular diastolic function and Ca2+ content of myocardial and cerebral mitochondria and artery tissues in left ventricular hypertrophied rats].

Left ventricular hypertrophy (LVH) was induced by renal hypertension in rats. m-Nifedipine (m-Nif, ig 20 mg.kg-1.d-1 for 9 wk) decreased LV weight in the renovascular hypertensive rats (P < 0.01). The LV compliance in LVH group was significantly decreased compared with that in sham- operated group. The LV stiffness constant, Ca2+ content in left ventricular myocardial and cerebral mitochondria, aorta, and tail artery were markedly raised. m-Nif could markedly reduce the LV stiffness constant, improve the LV compliance, and decrease the Ca2+ content of left ventricular myocardial mitochondria and tissues of artery from LVH rats. These effects of m-Nif were similar to those of nifedipine at the same dosage.

Animals↗

PubMed1978

Electrocardiographic criteria of left ventricular hypertrophy in left bundle-branch block.

In order to determine whether the electrocardiographic criteria of left ventricular hypertrophy apply in the presence of left bundle-branch block we studied 79 cases of intermittent left bundle-branch block and compared the QRS voltage and axis before and after its onset. Cases of incomplete left bundle-branch block were excluded. There was a statistically significant correlation between pre- and post-left bundle-branch block values of R or S wave voltage in leads I, V1, V2, V5, and V6, the Sokolow index (R V5 or V6 + S V1), and the QRS axis. There was a statistically significant reduction in R wave voltage in leads I, V5, and V6, an increase in S wave voltage in V1 and V2, and leftward shift of QRS axis, but the Sokolow index remained unchanged, after the onset of left bundle-branch block. The Sokolow criteria for left ventricular hypertrophy apply satisfactorily even in the presence of left bundle-branch block, though specificity is low, but QRS axis is unhelpful.

Bundle-Branch Block↗