Hemodynamic effects of verapamil in children and adolescents with hypertrophic cardiomyopathy.

Spicer, Robert L.; Rocchini, Albert P.; Crowley, Dennis C.; Vasiliades, John; Rosenthal, Amnon

doi:10.1161/01.cir.67.2.413

Cited by 44 publications

(7 citation statements)

References 30 publications

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“…Most published data regarding verapamil use in children concern patients with either hypertrophic cardiomyopathy [99,100] or arrhythmias [101]. Doses utilized for these indications have ranged from 3 to 5 mg/kg/day and appear to be well tolerated, although effects on blood pressure were not always reported.…”

Section: First-generation Ccbs: Verapamil Diltiazem and Nifedipinementioning

confidence: 99%

Calcium channel blockers: pharmacology and place in therapy of pediatric hypertension

Flynn

Pasko

2000

Pediatric Nephrology

106

104

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The calcium channel blockers (CCBs) are a diverse group of antihypertensive medications with variable pharmacokinetics and clinical effects. Although CCBs have been widely applied to the treatment of hypertensive children, data regarding the pharmacokinetics, efficacy and safety of these agents in children are extremely limited. In this review we briefly summarize the mechanism of action of CCBs and then summarize pertinent pharmacokinetic information on each of the CCBs commonly used in children, including amlodipine, diltiazem, felodipine, isradipine, intravenous nicardipine, nifedipine and verapamil. Clinically important drug interactions and adverse effects are discussed, as well as the potential role of CCBs in renal protection. Available pediatric efficacy and safety data are summarized, and recommendations made regarding the rational use of CCBs in the management of pediatric hypertension.

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Section: First-generation Ccbs: Verapamil Diltiazem and Nifedipinementioning

confidence: 99%

Calcium channel blockers: pharmacology and place in therapy of pediatric hypertension

Flynn

Pasko

2000

Pediatric Nephrology

106

104

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“…The acute hemodynamic effects of intravenous verapamil in 9 of these patients have been described. 3 At cardiac catheterization, LV outflow obstruction at rest greater than 10 mm Hg was present in 8 of 13 patients. These 8 patients had a peak systolic ejection gradient of 30 to 139 mm Hg (mean 74) after provocation with isoproterenol, Valsalva maneuver, premature ventricular contractions or exercise testing as previously described.…”

Section: Subjectsmentioning

confidence: 94%

Chronic verapamil therapy in pediatrie and young adult patients with hypertrophic cardiomyopathy

Spicer

Rocchini

Crowley

et al. 1984

The American Journal of Cardiology

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Oral verapamil, 5.2 +/- 1.1 mg/kg/day (range 2.8 to 7), was administered to 13 pediatric patients with hypertrophic cardiomyopathy for 13 +/- 6 months (range 2 to 20). The patients had significant symptomatic improvement on verapamil therapy. Murmur intensity diminished in 6 patients during therapy and left ventricular (LV) electromotive forces on the electrocardiogram diminished in 4, increased in 5 and did not change in 4. Exercise endurance increased from 8.4 +/- 3.9 to 10.9 +/- 2.8 minutes (p less than 0.01). Seven patients had ST-segment depression (0.38 +/- 0.28 mV) before verapamil therapy, which improved after verapamil therapy in 5 (0.24 +/- 0.17 mV, p less than 0.02). Of 4 patients with exercise-induced ventricular ectopic activity, 3 had diminution or abolishment of ectopy following verapamil. By echocardiography, the patients had an increase in LV end-diastolic dimension from 3.4 +/- 0.7 to 3.9 +/- 0.8 cm (p less than 0.01), with no significant change in shortening fraction (46.1 +/- 8.0% vs 44.6 +/- 8.0%). When adjusted for body size and age there was a significant decrease in LV septal thickness (from 106 +/- 70 to 45 +/- 52% of predicted normal values, p less than 0.05) and LV posterior wall thickness (from 40 +/- 45 to 5 +/- 26% of predicted normal values p = 0.05) after verapamil. Isovolumic relaxation time decreased from 69 +/- 26 to 42 +/- 19 ms after verapamil (p less than 0.01). Systolic anterior motion of the anterior mitral leaflet disappeared in 5 of 8 patients and midsystolic closure of the aortic valve was no longer present in 4 of 8.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…If ß-blockers alone are ineffective, disopyramide can be added, titrated up to a maximum tolerated dose [127,128] because can abolish basal LV outflow pressure gradients and improve exercise tolerance and functional capacity without pro-arrhythmic effects [129][130][131]. Verapamil or ditiazem can be used when ß-blockers are contraindicated or ineffective [132][133][134][135]. Patients with HOCM (gradient ≥50 mm Hg,) and drug-refractory symptoms benefit from septal reduction therapy (SRT).…”

Section: Hocmmentioning

confidence: 99%

Hypertrophic Cardiomyopathy: Genetics, Pathogenesis, Diagnosis, Clinical Course and Therapy

Lazzeroni¹,

Centorbi²

2021

Cardiomyopathy - Disease of the Heart Muscle

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Hypertrophic cardiomyopathy (HCM) is a genetic disorder of cardiac myocytes that is characterized by cardiac hypertrophy, unexplained by the loading conditions, a non-dilated left ventricle and a normal or increased left ventricular ejection fraction (LV-EF). Prevalence of HCM has been estimated at 0.16% to 0.29% (≈ 1:625–1:344 individuals) in the general adult population. HCM represents the most common genetic heart disease and represent an archetypical single gene disorder with an autosomal dominant pattern of inheritance and historically termed a “disease of the sarcomere”. The precise mechanisms by which sarcomere variants result in the clinical phenotype have not been fully understood. Mutant sarcomere genes trigger several myocardial changes, leading to hypertrophy and fibrosis, which ultimately result in a small, stiff ventricle with impaired systolic and diastolic performance despite a preserved LV-EF. The most common differential diagnosis challenges in the presence of hypertrophic heart disease are represented by: athlete’s heart, hypertensive heart and other cardiomyopathies mimicking HCM. A multimodality approach using ECG, echocardiography, CMR, cardiac computed tomography (CCT) and cardiac nuclear imaging provides unique information about diagnosis, staging and clinical profiles, anatomical and functional assessment, metabolic evaluation, monitoring of treatment, follow-up, prognosis and risk stratification, as well as preclinical screening and differential diagnosis. HCM may be associated with a normal life expectancy and a very stable clinical course. However, about a third of patients develop heart failure (HF); in addition, 5–15% of cases show progression to either the restrictive or the dilated hypokinetic evolution of HCM, both of which may require evaluation for cardiac transplantation. The clinical course of HCM has been classified into four clinical stages: non-hypertrophic, classic, adverse remodeling and overt dysfunction phenotype. No evidence-based treatments are available for non-hypertrophic HCM patients (pre-hypertrophic stage), on the other hand in classic HCM, adverse remodeling and overt dysfunction phenotype, pharmacological or interventional strategies have the target to improve functional capacity, reduce symptoms, prevent disease progression. Therapeutic approach mainly differs on the basis of the presence or absence of significant obstructive HCM. Adult patients with HCM report an annual incidence for cardiovascular death of 1–2%, with sudden cardiac death (SCD), HF and thromboembolism being the main causes of death; the most commonly recorded fatal arrhythmic event is spontaneous ventricular fibrillation. For this reason, SCD risk estimation is an integral part of clinical management of HCM. International guidelines suggest the evaluation of several risk factor for SCD based on personal and family history, non-invasive testing including echocardiography, ambulatory electrocardiographic 24 hours monitoring and CMR imaging in order to identity those patients most likely to benefit implantable cardioverter-defibrillator (ICD) implantation. The present chapter summarize genetics, pathogenesis, diagnosis, clinical course and therapy of HCM as well as novel therapeutic options.

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Hemodynamic effects of verapamil in children and adolescents with hypertrophic cardiomyopathy.

Cited by 44 publications

References 30 publications

Calcium channel blockers: pharmacology and place in therapy of pediatric hypertension

Calcium channel blockers: pharmacology and place in therapy of pediatric hypertension

Chronic verapamil therapy in pediatrie and young adult patients with hypertrophic cardiomyopathy

Hypertrophic Cardiomyopathy: Genetics, Pathogenesis, Diagnosis, Clinical Course and Therapy

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