scholarly journals Apical hypertrophic cardiomyopathy associated with circumflex to left ventricular fistulae: a case report of two rare subtypes of rare conditions occurring together

2021 ◽  
Vol 5 (2) ◽  
Author(s):  
Samuel Conway ◽  
Anna S Herrey ◽  
Roby D Rakhit
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Systolic Function ◽  
Beta Blockers ◽  
Left Ventricular ◽  
Wave Inversion ◽  
Cardiac Symptoms ◽  
Coronary Steal ◽  
Artery Disease ◽  
Apical Hypertrophy ◽  
Cavity Obliteration

Abstract Background  Coronary arterial fistulae are rare yet have been associated with hypertrophic cardiomyopathy (HCM). We present a patient who was found to have a left circumflex (LCx) to left ventricular (LV) fistula in combination with apical HCM. Case summary  A 72-year-old female presented with syncope after exercise. She sustained facial injuries including fracture of her nasal bones. There were no previous episodes, no cardiac history, and she denied chest pain or anginal symptoms. Electrocardiogram showed sinus rhythm with T-wave inversion throughout the chest leads. Echocardiography suggested apical HCM with hypertrophy of the LV apex but good systolic function. This was confirmed on cardiac magnetic resonance imaging with a characteristically spade-shaped LV cavity. Coronary angiography demonstrated a distal LCx to LV fistula from the apical hypertrophy but no coronary artery disease. She was started on beta-blockers and has had no further episodes, remaining well. Discussion  Coronary fistulae are present in 0.002% of the population but clinical outcomes are poorly understood. The majority are asymptomatic but anginal chest pains can occur through the ‘coronary steal’ phenomenon. Apical HCM is a subtype of HCM characterized by spade-shaped LV cavity obliteration. It is unclear whether the association between fistulae and HCM occur because of the increased vascularization and fibrosis associated with HCM or whether congenital malformation leads to hypertrophy. Both can produce a constellation of cardiac symptoms. Our patient has the previously unreported combination of apical HCM and an LCx fistula; two rarer subtypes of rare conditions appearing together.

Apical hypertrophic cardiomyopathy: what are the risks in our diverse military population?

2018 ◽  
Vol 165 (3) ◽  
pp. 206-209
Author(s):  
Leanne Jane Eveson ◽  
A Williams
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Normal Sinus Rhythm ◽  
Cardiopulmonary Exercise Testing ◽  
Left Ventricular ◽  
Inferior Wall ◽  
Military Population ◽  
Apical Hypertrophic Cardiomyopathy ◽  
Normal Sinus ◽  
Wave Inversion ◽  
Apical Hypertrophy

We present the case of a 50-year-old, fit, asymptomatic gurkha officer. At a routine medical, an ECG showed T-wave inversion in the chest leads V3–6. Transthoracic echo showed left ventricular apical hypertrophy and cavity obliteration consistent with apical hypertrophic cardiomyopathy (ApHCM). Cardiac magnetic resonance imaging showed apical and inferior wall hypertrophy in the left ventricle with no aneurysm or scarring. A 24-hour monitor showed normal sinus rhythm with no evidence of non-sustained ventricular tachycardia. Eighteen-panel genetic testing revealed no specific mutations. Cardiopulmonary exercise testing demonstrated a V̇O2 max, anaerobic threshold and peak V̇O2 consistent with above average cardiopulmonary capacity. There was no family history of either ApHCM or sudden cardiac death (SCD). Risk of SCD by the European Society of Cardiology’s HCM calculator was low. This case generates discussion on the prognosis of ApHCM, factors that worsen prognosis, occupational limitation considerations and appropriate monitoring in this patient group.

Value of a comprehensive exercise echocardiography assessment for patients with hypertrophic cardiomyopathy

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
J.C Peteiro Vazquez ◽  
J Peteiro ◽  
R Barriales-Villa ◽  
J Larranaga-Moreira ◽  
C Martinez-Veira ◽  
...  
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Diastolic Function ◽  
Wall Thickness ◽  
Systolic Function ◽  
Beta Blockers ◽  
Left Ventricular ◽  
Exercise Echocardiography ◽  
Metabolic Equivalents ◽  
Lv Systolic Function ◽  
Systolic And Diastolic Function

Abstract Background Exercise echocardiography (ExE) may assess left ventricular (LV) systolic and diastolic function, LV outflow tract (LVOT) obstruction and mitral regurgitation (MR). We aimed to assess the feasibility and prognostic value of the assessment of all these issues during exercise in patients with hypertrophic cardiomyopathy (HCM). Methods LV systolic and diastolic function, LVOT gradients, and MR were evaluated during ExE in 285 patients with HCM (age 60±14 years, 168 men) and preserved LVEF (≥50%). Recordings were obtained at rest and peak exercise for regional/global LV systolic function and at rest and within 1.5 min after exercise for the rest of assessments: LVOT gradients, MR and ratio of early LV inflow velocity to early tissue Doppler septal annulus velocity (E/e'). Results Feasibility was 100%, 97%, 98% and 98% for LV systolic function, E/e', LVOT gradients, and MR assessments at exercise, respectively. Thirty-seven patients (13%) had LVOT obstruction at rest, and 76 (27%) developed exercise-induced LVOT obstruction. Mean resting LVEF was 63±3%. New wall motion abnormalities (WMAs) were detected in 38 patients (13%). E/e'>15 was observed in 108 patients at rest (38%) and in 119 at exercise (42%). Corresponding figures for significant MR (moderate or severe) were 20 (7%) and 17 (6%). During follow-up of 3.9±2.5 years, 21 patients had a hard event (cardiac death or transplantation, appropriate discharge of a defibrillator, stroke, myocardial infarction, hospitalization for heart failure), 33 a combined event (hard plus new atrial fibrillation or syncope), and 53 a combined event plus any interventionism. After adjustment, LV wall thickness, resting LVEF, maximal workload in Metabolic Equivalents (METs), and E/e' post-exercise resulted independent predictors of hard events (HR=1.45, 95% CI: 1.21–1.74, p<0.001; HR=0.80, CI: 0.71–0.89, p<0.001; HR=0.73, 95% CI: 0.62–0.86, p<0.001; HR=1.08, 95% CI: 1.02–1.14, p<0.009, respectively). Independent predictors of combined events included also LV wall thickness, resting LVEF, and METs, along with therapy with beta-blockers at the time of ExE (HR=1.29, 95% CI: 1.12–1.50, p=0.001; HR=0.89, CI: 0.81–0.97, p=0.012; HR=0.83, 95% CI: 0.74–0.93, p=0.001; HR=2.51, 95% CI: 1.20–5.25, p=0.015), whereas the model for combined events+any interventionism consisted of beta-blockers, LV wall thickness, LA dimension, METs and new WMAs. (HR=2.15, 95% CI: 1.20–3.86, p=0.01; HR=1.17, 95% CI: 1.03–1.32, p=0.02; HR=1.07, CI: 1.02–1.11, p=0.005; HR=0.90, 95% CI: 0.82–0.98, p=0.01; HR=2.33, 95% CI: 1.17–4.63, p=0.016) Conclusions A comprehensive assessment during ExE is feasible for patients with HCM and provides significant incremental prognostic information Funding Acknowledgement Type of funding source: None

scholarly journals Heart rate-lowering therapy in gout patients with stable coronary artery disease: focus on ivabradine

2020 ◽  
Vol 25 (7) ◽  
pp. 3980
Author(s):  
N. N. Kushnarenko ◽  
T. A. Medvedeva ◽  
M. Yu. Mishko ◽  
T. M. Karavaeva
Keyword(s):  
Blood Pressure ◽  
Coronary Artery Disease ◽  
Heart Rate ◽  
Coronary Artery ◽  
Left Ventricular Systolic Dysfunction ◽  
Systolic Function ◽  
Beta Blockers ◽  
Left Ventricular ◽  
Controlled Study ◽  
Artery Disease

Aim. To study the effect of ivabradine and bisoprolol on cardiac hemodynamics and diastolic remodeling in gout patients with coronary artery disease and hypertension and without left ventricular systolic dysfunction.Material and methods. The open randomized parallel clinical trial of 35 men with intercritical gout at the age of 41,4±3,3 years, with class II-III stable angina, hypertension and sinus rhythm without data suggestive of heart failure was performed. All patients included in the study were randomly divided into two groups: eighteen patients took bisoprolol at a dose of 2,5 to 10 mg/day, 17 subjects received bisoprolol 2,5 mg/day with ivabradine (Coraxan, SERVIER, France) 5 mg 2 times a day. Adjustment of the therapy was carried out every 2 weeks until the target heart rate (HR) was reached at 55-60 beats/min and then remained unchanged until 12 weeks of therapy. All patients underwent echocardiography, 24-hour Holter and central aortic blood pressure monitoring, and 3-minute cycle ergometer test with a power of 25, 50, 75 and 100 watts.Results. There was a comparable decrease in the maximum and minimum 24-hour average heart rates in patients receiving only bisoprolol and those taking bisoprolol+ivabradine. Patients taking bisoprolol+ivabradine had a decrease of central systolic and diastolic blood pressure (BP). Pulse pressure in the bisoprolol group increased by 17,7% (p=0,02), and when ivabradine was added, on the contrary, it decreased by 7,0% (p=0,04). Twelve-week therapy with beta-blockers and ivabradine was accompanied by an effective decrease in the pulse wave velocity in both groups (p<0,05). All gout patients did not have a decrease of systolic function and there was an improvement in diastolic remodeling with beta-blockers and ivabradine therapy.Conclusion. The results obtained indicate that the addition of ivabradine to bisoprolol leads to an effective decrease in heart rate, an improvement in arterial stiffness and exercise tolerance. Combination therapy with ivabradine is accompanied by an improvement in clinical outcomes using lower doses of bet-blockers, which requires further study and a double-blind controlled study.

scholarly journals Intracoronary Injection of Autologous CD34+ Cells Improves One-Year Left Ventricular Systolic Function in Patients with Diffuse Coronary Artery Disease and Preserved Cardiac Performance—A Randomized, Open-Label, Controlled Phase II Clinical Trial

2020 ◽  
Vol 9 (4) ◽  
pp. 1043 ◽  
Author(s):  
Pei-Hsun Sung ◽  
Yi-Chen Li ◽  
Mel S. Lee ◽  
Hao-Yi Hsiao ◽  
Ming-Chun Ma ◽  
...  
Keyword(s):  
Systolic Function ◽  
Coronary Intervention ◽  
Left Ventricular ◽  
Diffuse Coronary Artery Disease ◽  
Cd34 Cells ◽  
Group 2 ◽  
Artery Disease ◽  
One Year ◽  
Lv Systolic Function ◽  
Group 1

This phase II randomized controlled trial tested whether intracoronary autologous CD34+ cell therapy could further improve left ventricular (LV) systolic function in patients with diffuse coronary artery disease (CAD) with relatively preserved LV ejection fraction (defined as LVEF >40%) unsuitable for coronary intervention. Between December 2013 and November 2017, 60 consecutive patients were randomly allocated into group 1 (CD34+ cells, 3.0 × 107/vessel/n = 30) and group 2 (optimal medical therapy; n = 30). All patients were followed for one year, and preclinical and clinical parameters were compared between two groups. Three-dimensional echocardiography demonstrated no significant difference in LVEF between groups 1 and 2 (54.9% vs. 51.0%, respectively, p = 0.295) at 12 months. However, compared with baseline, 12-month LVEF was significantly increased in group 1 (p < 0.001) but not in group 2 (p = 0.297). From baseline, there were gradual increases in LVEF in group 1 compared to those in group 2 at 1-month, 3-months, 6-months and 12 months (+1.6%, +2.2%, +2.9% and +4.6% in the group 1 vs. −1.6%, −1.5%, −1.4% and −0.9% in the group 2; all p < 0.05). Additionally, one-year angiogenesis (2.8 ± 0.9 vs. 1.3 ± 1.1), angina (0.4 ± 0.8 vs. 1.8 ± 0.9) and HF (0.7 ± 0.8 vs. 1.8 ± 0.6) scores were significantly improved in group 1 compared to those in group 2 (all p < 0.001). In conclusion, autologous CD34+ cell therapy gradually and effectively improved LV systolic function in patients with diffuse CAD and preserved LVEF who were non-candidates for coronary intervention (Trial registration: ISRCTN26002902 on the website of ISRCTN registry).

Abstract P024: Pharmacological Treatment of Hypertension and Lv Dysfunction Predictors in ESRD Patients With AV Fistula

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Sayed Tariq ◽  
James Anderson ◽  
Rohit Dhingra ◽  
Mikhail Torosoff
Keyword(s):  
Systolic Function ◽  
Beta Blockers ◽  
Systolic Dysfunction ◽  
Left Ventricular ◽  
Channel Blockers ◽  
Ca Channel ◽  
Av Fistula ◽  
Fistula Surgery ◽  
Lv Dysfunction ◽  
Ca Channel Blockers

Background: Effects of anti-hypertensive medications on left ventricular dimensions and systolic function in patients with arterio-venous (AV) fistulas have not been well investigated. Material and Methods: Medical charts and echocardiograms of 346 patients with AV fistula were reviewed. Of 346, 149 patients had TTE prior to the AV fistula surgery, 197 had TTE after the AV fistula surgery, and 76 patients had TTE before and after the AV fistula surgery. Data on medication use was available in 314 patients. ANOVA, chi-square, and logistic regression tests were employed. Results: In patients scheduled for AV fistula placement, 20% (31/149) patients had systolic dysfunction and 15% (22/142) had increased LV end-diastolic dimensions (LVEDD). Moderate systolic LV dysfunction was observed in 6% (9/149) and additional 8% (12/149) had severe LV dysfunction. Increased LVEDD with some LV dysfunction was noted in 27% (38/142).Following the AV fistula placement, 18% (36/197) of patients had systolic dysfunction and 12% (22/187) had increased LV end-diastolic dimensions (LVEDD). Moderate or severe systolic LV dysfunction was observed in 6% (5/197). LV systolic dysfunction or dilatation was noted in 23% (43/187). Of 314 patients, 63% were on beta-blockers (BB), 25% were on ACE inhibitor or an ARB , 43% on calcium-channel blocker , and 15% on alpha-antagonist . BB, ACEi-ARB, or AA were not associated with increased LVEDD or systolic dysfunction before or after the AV fistula placement. Prior to AV fistula, CCB treatment was not related to LV dilatation (36% in each group, p=0.981) Post AV fistula, CCB treatment was associated with increased LV dimensions (71% vs. 46%, p=0.029) but not LV systolic dysfunction (49% in LV dysfunction vs. 38% in the rest, p=0.446) . This association persisted after adjustment for co-morbidities and demographic parameters. Conclusions: LV systolic dysfunction and/or dilatation are common in patients undergoing AV fistula surgery. Despite decreased use of Ca-channel blockers in patients with LV dysfunction prior to AV fistula, Ca-channel blockers are associated with increased LV dimensions post AV fistula, and probably should be avoided in this vulnerable patient population.

scholarly journals CORONARY ARTERY DISEASE

2009 ◽  
Vol 16 (02) ◽  
pp. 192-197
Author(s):  
FIDA MUHAMMAD ◽  
Nadeem Hayat Mallick, ◽  
ABDUL REHMAN ABID ◽  
AJAZ AHMAD ◽  
Shahid Imran
Keyword(s):  
Coronary Artery Disease ◽  
Risk Factor ◽  
Coronary Artery ◽  
Clinical Presentation ◽  
Systolic Function ◽  
Left Ventricular ◽  
Premature Coronary Artery Disease ◽  
Common Risk Factor ◽  
Artery Disease ◽  
Lv Systolic Function

Objectives: This study was designed to evaluate the pattern of clinical presentation, risk factors and angiographic findingsin young males presenting with acute myocardial infarction (AMI).Materials and methodsThis cross-sectional descriptive study wasconducted at the Cardiology Department, Punjab Institute of Cardiology, Lahore from May 2005 till February 2006. After fulfilling the inclusioncriteria 200 male patients <40 years with coronary artery disease (CAD) were studied. Results: Mean age of the study population was31.5±9.2 years with an age range of 31 to 40 years. Most common risk factor was smoking present in 60% patients. Family history ofischemic heart disease (IHD) was present in 44.5% patients, hyperlipidemia in 35.5% patients, hypertension in 25.5% and diabetes mellitusin 17.5% of patients.Common mode of clinical presentation was AMI 42.5% patients. Left anterior descending (LAD) was diseased in 73.5%,followed by Left Circumflex (LCx) 51% and Right Coronary Artery (RCA) in 39% patients. Left Main Stem (LMS) disease occurred in 9.5%patients. Good left ventricular (LV) systolic function was observed in 38%, moderate LV systolic function in 34% and poor LV systolic functionin 14.5% patients. Conclusion: Patients with premature coronary artery disease have unheralded acute onset of symptoms. Smoking isthe most common risk factor. Young patients have single vessel CAD with frequent involvement of LAD and commonly have good leftventricular systolic function.

scholarly journals Tachycardia-induced myocardial ischemia and diastolic dysfunction potentiate secretion of ANP, not BNP, in hypertrophic cardiomyopathy

2006 ◽  
Vol 290 (3) ◽  
pp. H1064-H1070 ◽  
Author(s):  
Shinsuke Kido ◽  
Naoyuki Hasebe ◽  
Yoshinao Ishii ◽  
Kenjiro Kikuchi
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Myocardial Ischemia ◽  
Diastolic Dysfunction ◽  
Diastolic Pressure ◽  
Systolic Function ◽  
Left Ventricular ◽  
Atrial Pacing ◽  
Catheter Tip ◽  
Lv Systolic Function ◽  
Lv Diastolic Dysfunction

The aim of this study was to investigate what factor determines tachycardia-induced secretion of atrial and brain natriuretic peptides (ANP and BNP, respectively) in patients with hypertrophic cardiomyopathy (HCM). HCM patients with normal left ventricular (LV) systolic function and intact coronary artery ( n = 22) underwent rapid atrial pacing test. The cardiac secretion of ANP and BNP and the lactate extraction ratio (LER) were evaluated by using blood samples from the coronary sinus and aorta. LV end-diastolic pressure (LVEDP) and the time constant of LV relaxation of tau were measured by a catheter-tip transducer. These parameters were compared with normal controls ( n = 8). HCM patients were divided into obstructive (HOCM) and nonobstructive (HNCM) groups. The cardiac secretion of ANP was significantly increased by rapid pacing in HOCM from 384 ± 101 to 1,268 ± 334 pg/ml ( P < 0.05); however, it was not significant in control and HNCM groups. In contrast, the cardiac secretion of BNP was fairly constant and rather significantly decreased in HCM ( P < 0.01). The cardiac ANP secretion was significantly correlated with changes in LER ( r = −0.57, P < 0.01) and tau ( r = 0.73, P < 0.001) in HCM patients. Tachycardia potentiates the cardiac secretion of ANP, not BNP, in patients with HCM, particularly when it induces myocardial ischemia and LV diastolic dysfunction.

Sign in / Sign up

Export Citation Format

Share Document