A young male patient with an aortic systolic murmur that increases with the Valsalva maneuver and signs of left ventricular enlargement is practically a "portrait" of the typical findings that can be found in hypertrophic cardiomyopathy. Very easy question.

A young male patient with an aortic systolic murmur that increases with the Valsalva maneuver and signs of left ventricular enlargement is practically a "portrait" of the typical findings that can be found in hypertrophic cardiomyopathy. [HIDDEN]

A 26-year-old man with no history of interest, asymptomatic, presents on examination with a mesosystolic murmur in the aortic focus and left parasternal border that increases with the Valsalva maneuver. BP and peripheral pulses are normal and the ECG shows signs of marked left ventricular enlargement and very deep negative T waves in V3, V4, V5 and V6. What is the most likely diagnosis?

[Deep Q waves in the ECG of children--an electro-, vector- and echocardiographic study].

Out of 9557 children we found 120 children (1,26%), who showed deep Q-waves of greater than or equal to 0.4 mV in 3 consecutive ECG's at least in one of the leads I, aVL, V4, V5 and V6. 70 children were investigated additionally by echocardiography, 45 by vectorcardiography according to Frank. Echocardiography revealed an increased septal thickness in 5 patients, a borderline thickness in 8, an increased septal/posterior wall ratio in 4. In the vectorcardiogram 51,1% of the patients had no Q-waves in lead y, mostly in combination with deep Q-waves in a VL or left axis deviation. Q-waves in lead y were combined with Q-waves in V 5/6. The determination of the main axis coincided in 80% of ECG and VCG. Looking for the various heart diseases, 30% of the children with Q-waves had a ventricular septal defect, 23,3% an endocardial cushion defect, 10,8% a patent ductus arteriosus, 3,3% a bradycardia, 2,5% a Bland-White-Garland syndrome and 1,6% a hypertrophic cardiomyopathy. 17,5% of the children had an innocent heart murmur, 5,8% no cardiac symptoms. Other diseases were found in 5%. The most frequent cause of Q-waves in children were volume-overload of the left ventricle (35%) and left axis deviation (33,3%), whereas myocardial infarction and septal hypertrophy (3,3 and 4,1%) were of minor importance. In healthy children (23,3%) we could not find any pathomechanism.

Electrocardiographic evolution in patients with hypertrophic cardiomyopathy who develop a left ventricular apical aneurysm.

Hypertrophic cardiomyopathy (HCM) patients with apical aneurysm have a largely unfavourable clinical course, and are often unrecognised because echocardiography is limited in the assessment of the left ventricular (LV) apex. The aim of this study is the identification of electrocardiographic (ECG) abnormalities associated with the development of apical aneurysm in HCM patients. Electrocardiographic features were assessed in 14 HCM patients who had a good-quality baseline ECG recorded before and after the diagnosis of apical aneurysm. During follow-up (8.8±7.5years), the following ECG changes were observed: increase in QRS-complex duration (87±12ms to 118±34ms, p=0.006), QRS-complex fragmentation, decrease in QRS-complex amplitude (SV1+RV5-6, from 41±18mm to 26±11mm, p=0.015), ST-segment elevation in V4-V6 (J-point in V5, from -0.9±1.3mm to +0.7±1.3, p=0.003), positivisation of negative T waves in V3-V6 (T-wave depth in V5, from -3.4±6.6 to +3.1±4.1, p=0.005). HCM patients who develop LV apical aneurysm exhibit distinctive ECG changes along with apical remodelling. Suggestive ECGs should lead the physician to study LV apex by nonstandard echocardiographic views, and perform MRI.

Electrocardiographical case. Asymptomatic patient with deep T-wave inversions.

A 45-year-old man was found to have an abnormal myocardial perfusion scan. He was asymptomatic, with no chest pain, breathlessness or palpitations. Clinical examination was unremarkable. The 12-lead electrocardiography (ECG) showed increased QRS voltage in leads V3-V6, and deep T-wave inversions noted in leads V3-V6, with an absence of septal Q waves. These ECG features were characteristic of apical variant hypertrophic cardiomyopathy (HCM). He underwent a coronary angiogram that revealed normal coronary arteries, and a left ventriculogram which showed apical HCM. Transthoracic echocardiography further confirmed the diagnosis. No drug therapy was instituted as he was asymptomatic. Apical HCM is discussed.

[Use of systolic times and electrocardiography for the evaluation of left ventricle involvement in aortic valve diseases].

75 patients suffering from aortic valvulopathy without signs of left ventricular insufficiency have been examined. Left ventricular function is studied by determining systolic times with polygraphic examination (Q-S2, LVET and PEP). The ECG findings were assessed with a myocardial hypertrophy criterion based on a point-score system. Finally, the time of total carotidogram ascent, the 1/2 T and the distance between Q wave and acme of the systolic murmur (Q-acme) were measured. It is concluded that: 1) The most meaningful increases in LVET are associated with the most evident shortenings in PEP only in the phase of the disease in which left ventricular hypertrophy is at its height. 2) The delay in systolic wave ascent should be considered indicative of the functional haemodynamic importance of aortic stenosis, whereas the earliness or otherwise of systolic murmur acme is an expression of the anatomic extent of the stenosis in question.

[Hypertrophic cardiomyopathy with progressive left ventricular hypertrophy: a case report].

A 64-year-old man was hospitalized in March 1983 for recurrent episodes of dyspnea and palpitation despite medical treatment. At 48 years of age (1967), hypertension was diagnosed, but well controlled by propranolol. At the age of 59 years (1979), his first episode of dyspnea and palpitation was noted, with electrocardiographic (ECG) evidence of left ventricular hypertrophy (LVH), and abnormal Q waves in leads III and a VF. The echocardiogram, however, showed mild LVH with neither asymmetric septal hypertrophy (ASH) nor systolic anterior movement (SAM). On admission (1983), his blood pressure was 130/70 mmHg, and a grade III systolic murmur was heard along the left sternal border and over the apex. On ECG, the left precordial voltage (Sv1 + Rv5) was diminished and the depth of the Q wave in lead III increased compared with that of 1978. On echocardiography, we observed prominent septal hypertrophy (IVST: 20 mm) with ASH (IVST/PWT = 2.0), SAM, an enlarged left atrium, and a diminished left ventricular (LV) cavity. Left ventricular catheterization showed a pressure gradient of 90 mmHg between the LV apex and outflow tract and histological examination of the bi-ventricular endomyocardial biopsy material showed markedly hypertrophied and mildly disarranged myocardial fibers with bizarre nuclei. We considered that this was an interesting case in which ASH and SAM developed in the progression of LVH during the follow-up period.

Heart murmur

Tricuspid valve regurgitation presents as a holosystolic (pansystolic) murmur at the left lower sternal border with radiation to the left upper sternal border. Prominent v and c waves may be seen in the JVP (jugular venous pressure). The murmur will increase with inspiration. Hypertrophic obstructive cardiomyopathy (or hypertrophic subaortic stenosis) will be a systolic crescendo-decrescendo murmur best heard at the left lower sternal border. Valsalva maneuver will increase the intensity of the murmur, as will changing positions from squatting to standing. Atrial septal defect will present with a systolic crescendo-decrescendo murmur best heard at the left upper sternal border due to increased volume going through the pulmonary valve, and is associated with a fixed, split S2 and a right ventricular heave.

T wave

Hypertrophic cardiomyopathy is the thickening of the left ventricle, occasionally right ventricle. It may be associated with left ventricular outflow tract obstruction or may not be associated with it in 75% of the cases. ECG would be abnormal in 75 to 95% of the patients. Characteristic ECG changes would be large QRS complex associated with giant T wave inversion in lateral leads I, aVL, V5, and V6, together with ST segment depression in left ventricular thickening. For right ventricular thickening, T waves are inverted from V1 to V3 leads. ST and T waves changes may not be apparent in hypertrophic cardiomyopathy, but if there is presence of ST and T waves changes indicates severe hypertrophy or ventricular systolic dysfunction. According to Sokolow-Lyon criterion, the height of R wave in V5 or V6 + the height of S wave in V1 more than 35 mm would be suggestive of left ventricular hypertrophy.

[Repeated changes of electrocardiogram caused by Takotsubo-type cardiomyopathy: a case with hypertrophic nonobstructive cardiomyopathy].

A 67-year-old woman had been examined due to abnormalities on electrocardiography (ECG) at a medical checkup three years previously. When a negative T-wave was seen in leads I, aVL, and V1 to V4, but the abnormal findings were improved at consultation. Echocardiography revealed apical hypertrophy and hypertrophic nonobstructive cardiomyopathy was diagnosed. She felt chest discomfort in September, 2003 and an ECG showed a negative T-wave in leads I, II, III aVL, aVF and V2 to V6 and an elongation of QT interval Left ventriculography revealed myocardial hypertrophy at the left ventricular apex and left ventriclar wall motion was normal. Coronary angiography did not show any significant luminal narrowing. I-123 metaiodobenzyl-guanitidine scintigraphy showed marked perfusion defects at the left ventricular apex. After five months, ECG showed an improvement of the QT interval and a decrease in the negative T-wave. We considered that the repeated changes of ECG were caused by Takotsubo-type cardiomyopathy.

[Regression of giant negative T waves in hypertrophic cardiomyopathy: cases simulating either dilated cardiomyopathy or severe coronary artery stenosis].

Two cases of hypertrophic cardiomyopathy (HCM), in whom giant negative T waves resolved during 10 years, are reported. Case 1: A 33-year-old man was admitted in 1975 for careful evaluation because of an ECG abnormality. The ECG revealed a giant negative T wave (GNT) in V5 (-15 mm) and high voltage (SV1 + RV5 = 81 mm). The thickness of the apical wall was 18 mm; the anterior wall, 12 mm; the posterior wall, 16 mm; and the interventricular septum, 17 mm on the left ventriculogram and biventriculogram. The coronary angiogram was normal. From these data, this patient was diagnosed as having HCM. However, follow-up studies disclosed resolution of the GNT with decreased high voltage (SV1 + RV5 = 26 mm). The catheterization performed in 1985 showed a decrease of wall thickness: the apical wall to 10 mm; the anterior wall, 9 mm; the posterior wall, 14 mm; and the interventricular septum, 14 mm. Ejection fraction was markedly decreased from 79.8% to 27.1%, and the wall motion was generally reduced. The coronary angiogram was normal. These findings resemble the clinical pictures of dilated cardiomyopathy (DCM). Case 2: A 58-year-old man was admitted in 1974 because of easy fatiguability. His ECG revealed a GNT in V4 (-10 mm) and high voltage (SV1 + RV5 = 75 mm). The patient was diagnosed as having HCM by cardiac catheterization, right ventricular biopsy and other procedures. In 1985, the depth of the GNT and the voltage of SV1 + RV5 regressed significantly (SV1 + RV5 = 26 mm). The thickness of the apical wall was, 12 mm; the anterior wall, 19 mm; the posterior wall, 13 mm; and the interventricular septum 14 mm during recatheterization. Coronary angiography disclosed stenoses of the left main trunk (75%), the left anterior descending artery (99%) and the left circumflex artery (50%). The right coronary artery was totally occluded. In conclusion, these two cases of HCM had similar changes in their ECG during long-term follow-up studies, but the process was different. One case finally showed clinical pictures of DCM; the other, severe coronary stenoses. These suggested that blood flow to the myocardium is an important determinant for the development of clinical features simulating DCM in cases with HCM.

[Electrocardiography in cardiomyopathies].

ECG plays a predominantly screening role in cardiomyopathies. It is particularly important in hypertrophic cardiomyopathies, where atrial abnormities may be present (25%), positive voltage criteria in hypertrophy of the left ventricle (63%), pathological Q or QS wave (24%), missing septal q in V5 and V6 (49%), missing increase in the R wave in V1-V3 (29%) and high R waves in V2-V3 (15%), changes in repolarization phase of the ST-T segment (87%). The left Tawar arm blockade is particularly typical for dilatation cardiomyopathies. In arrhythmogenic cardiomyopathies of the right ventricle the epsilon ware can be found as well as negative T waves in the leads from the right precordium and ventricular arrhythmias in the shape of the left Tawar arm blockade.

Heart murmur

Ventricular septal defect (VSD) will present as a holosystolic (pansystolic) murmur at the left lower sternal border, associated with a palpable thrill, and increases with isometric handgrip. A right to left shunt (Eisenmenger syndrome) may develop with uncorrected VSDs due to worsening pulmonary hypertension, which will increase the murmur intensity and be associated with cyanosis. Flow murmur may be heard at the right upper sternal border in certain conditions, such as anemia, hyperthyroidism, fever, and pregnancy. Diastolic Aortic valve regurgitation will present as a diastolic decrescendo murmur heard at the left lower sternal border or right lower sternal border (when associated with a dilated aorta). This may be associated with bounding carotid and peripheral pulses (Corrigan's pulse, Watson's water hammer pulse), and a widened pulse pressure.

List of cardiology mnemonics

Renal failure Embolism: pulmonary Complications of Myocardial Infarction Darth Vader Death Arrythmia Rupture(free ventricular wall/ ventricular septum/ papillary muscles) Tamponade Heart failure (acute or chronic) Valve disease Aneurysm of Ventricles Dressler's Syndrome thromboEmbolism (mural thrombus) Recurrence/ mitral Regurgitation Coronary artery bypass graft: indications DUST:p. 31 Depressed ventricular function Unstable angina Stenosis of the left main stem Triple vessel disease ECG: left vs. right bundle block WiLLiaM MaRRoW:p. 31 W pattern in V1-V2 and M pattern in V3-V6 is Left bundle block. M pattern in V1-V2 and W in V3-V6 is Right bundle block. Exercise ramp ECG: contraindications RAMP:p. 31 Recent MI Aortic stenosis MI in the last 7 days Pulmonary hypertension Endocarditis FROM JANE: Fever Roth's spots Osler's nodes Murmur of heart Janeway lesions Anemia Nail hemorrhage Emboli Heart valve sequence Try Puling My Aorta:p. 3 Tricuspid

Valsalva maneuver

Medical diagnostics Cardiology The maneuver can sometimes be used to diagnose heart abnormalities, especially when used in conjunction with an echocardiogram. For example, the Valsalva maneuver (phase II) increases the intensity of hypertrophic cardiomyopathy murmurs, namely those of dynamic subvalvular left ventricular outflow obstruction. At the same time, the Valsalva maneuver (phase II) decreases the intensity of most other murmurs, including aortic stenosis and atrial septal defect. During the first few seconds of the Valsalva maneuver (phase I) the opposite findings will be the case.

Aortic stenosis

Other peripheral signs include: sustained, heaving apex beat, which is not displaced unless systolic dysfunction of the left ventricle has developed A precordial thrill narrowed pulse pressure Electrocardiogram Although aortic stenosis does not lead to any specific findings on the electrocardiogram (ECG), it still often leads to a number of electrocardiographic abnormalities. ECG manifestations of left ventricular hypertrophy (LVH) are common in aortic stenosis and arise as a result of the stenosis having placed a chronically high-pressure load on the left ventricle (with LVH being the expected response to chronic pressure loads on the left ventricle no matter what the cause).

Intracardiac Shunts -- Evaluation

After the initial history and physical examination, further workup should be done as warranted. The extent of evaluation for intracardiac shunts depends on a case-by-case basis and could include blood testing, EKG, echocardiogram, chest x-ray, CT scan, and cardiac catheterization. EKG could indicate signs of pulmonary hypertension from right ventricular hypertrophy (RVH), right axis deviation, and right atrial enlargement. RVH shows tall R wave in V1, dominant S wave in leads V5 and V6 and can also produce p pulmonale and right ventricular strain pattern on EKG that could be evidenced by ST depressions and T wave inversions in the right precordial (V1-V4) and inferior (II, III, aVF) leads. [10]

Palpitation -- History and Physical

Positive orthostatic vital signs may indicate dehydration or an electrolyte abnormality. A midsystolic click and murmur may indicate mitral valve prolapse.  A harsh holosystolic murmur best heard at the left sternal border which increases with Valsalva may indicate hypertrophic obstructive cardiomyopathy. Fixed splitting of the S2 throughout the cardiac cycle and a right ventricular heave are characteristic clinical features of the atrial septal defect. An irregular rhythm indicates atrial fibrillation or atrial flutter. Evidence of cardiomegaly and peripheral edema may indicate heart failure and ischemia or a valvular abnormality. [1] [2] [6]

Heart sounds

"ta-lub-dub" or "a-stiff-wall" It is a sign of a pathologic state, usually a failing or hypertrophic left ventricle, as in systemic hypertension, severe valvular aortic stenosis, and hypertrophic cardiomyopathy. The sound occurs just after atrial contraction at the end of diastole and immediately before S1, producing a rhythm sometimes referred to as the "Tennessee" gallop where S4 represents the "Ten-" syllable. It is best heard at the cardiac apex with the patient in the left lateral decubitus position and holding his breath. The combined presence of S3 and S4 is a quadruple gallop, also known as the "Hello-Goodbye" gallop. At rapid heart rates, S3 and S4 may merge to produce a summation gallop, sometimes referred to as S7. Atrial contraction must be present for production of an S4. It is absent in atrial fibrillation and in other rhythms in which atrial contraction does not precede ventricular contraction. Murmurs

Systolic ejection murmurs in the era of modern cardiology: what do we really know?

The basics of pulsatile ejection dynamics are reviewed in order to clarify the relationships among left ventricular and aortic pressures, intra-left ventricular and aortic flow velocities, and cardiovascular sound. The principles of turbulent flow are examined using the Reynolds number concept, and the evidence for cause-and-effect relationships between turbulent flow and murmur generation is presented. Examples of hemodynamics and phonocardiography are given for normal subjects and are compared to patients with aortic stenosis and hypertrophic cardiomyopathy. The concepts presented are used to analyze the results of a new study suggesting increased intraventricular velocities as a new cause for systolic murmurs in adults.

Handgrip maneuver

The handgrip maneuver is performed by clenching one's fist forcefully for a sustained time until fatigued. Variations include squeezing an item such as a rolled up washcloth. Physiological response The handgrip maneuver increases afterload by squeezing the arterioles and increasing total peripheral resistance. Cardiology Since increasing afterload will prevent blood from flowing in a normal forward path, it will increase any murmurs that are due to backwards flowing blood. This includes aortic regurgitation (AR), mitral regurgitation (MR), and a ventricular septal defect (VSD). Mitral valve prolapse: The click and the murmur of mitral valve prolapse are delayed because left atrial volume also increases due to mitral regurgitation along with increased left ventricular volume. Murmurs that are due to forward flowing of blood such as aortic stenosis, and hypertrophic cardiomyopathy decrease in intensity.

[Extreme cardiac hypertrophy in athletes. Morphological and functional echographic study].

Cardiac hypertrophy is an adaptation phenomenon of the heart as a result of increased hemodynamic load due to intense and prolonged training in athletes. This is mainly seen in endurance athletes. In some cases cardiac hypertrophy can mimic hypertrophic cardiomyopathy, specially if hypertrophy is mainly localized at the interventricular septum as compared to the left ventricular free wall. In our study we tried to evaluate the different diagnostic features obtained by echocardiography and clinical examination in a group of 23 athletes with marked hypertrophy (all were participants to the 1984 Olympic Games held in Los Angeles) as compared to a group of 11 sportsmen with non-obstructive hypertrophic cardiomyopathy (HC). Cardiomyopathy was diagnosed on the basis of clinical, echocardiographic and angio-scintigraphic findings. The 23 athletes were selected on the basis of M-Mode and 2D echocardiographic thickness of the interventricular septum (IVS) which was in diastole greater than or equal to 15 mm. They were all asymptomatic, only 4 of the 23 athletes had ECG anomalies due to left axis deviation (LAS) and T wave inversion. Only 4 of the subjects with HC had a family history of HC. ECG changes were the following: T wave inversion (9 subjects), left axis deviation (LAD) (4 subjects), deep Q wave in D2-3, aVF, V5-6 (2 subjects) and low voltage R wave in V5-6 (1 subject). All the athletes had marked hypertrophy of the IVS. Interventricular septum thickness (IVST) was 15.7 +/- 0.6 mm, with a range from 15 to 17.5 mm. Posterior wall thickness (PWT) was 13.7 +/- 1.1 with a range from 12 to 16 mm. The sportsmen with HC had an IVST of 16.2 +/- 3.5 mm and a PWT of 11.3 +/- 1.5 mm. The IVST/PWT ratio was significantly lower (p less than 0.01) in the athletes (1.14 +/- 0.02) when compared to the group with HC (1.4 +/- 0.3). In 7 of the subjects with HC the hypertrophy was mainly localized at the anterolateral segment of the interventricular septum (in 4 of these subjects the hypertrophy involved also the antero-lateral part of the left ventricular free wall).(ABSTRACT TRUNCATED AT 400 WORDS)

Aortic regurgitation

If there is increased stroke volume of the left ventricle due to volume overload, an ejection systolic 'flow' murmur may also be present when auscultating the same aortic area. Unless there is concomitant aortic valve stenosis, the murmur should not start with an ejection click. There may also be an Austin Flint murmur, a soft mid-diastolic rumble heard at the apical area; it appears when a regurgitant jet of blood from severe aortic regurgitation partially closes the anterior mitral leaflet. Peripheral physical signs of aortic regurgitation are related to the high pulse pressure and the rapid decrease in blood pressure during diastole due to blood returning to the heart from the aorta through the incompetent aortic valve, although the usefulness of some of the eponymous signs has been questioned: Phonocardiograms detect AI by having electric voltage mimic the sounds the heart makes. Characteristics- indicative of aortic regurgitation are as follow:

A pediatric case of hypertrophic cardiomyopathy with mid-ventricular obstruction incidentally detected by electrocardiography.

A 13-year-old girl was admitted to our hospital because mitral P wave and ST depression in leads II, III, aVF, and V3-6 were incidentally detected on electrocardiography at a school health examination. Although she had noted no cardiac symptoms during club volley ball games, the treadmill exercise test induced chest discomfort in the absence of obvious electrocardiographic changes. B-type natriuretic peptide was elevated at 685 pg/ml. Echocardiography revealed left mid-ventricular hypertrophy and obstruction, sparing of the apical ventricle at end-systole, and severe left atrial dilatation. Continuous-wave Doppler echocardiography clarified a peak pressure gradient of about 40 mmHg between the apical and basal sites of the left ventricle. Swan-Ganz catheterization suggested elevated atrial pressure and left ventricular end-diastolic pressure. Left ventriculography showed an "hourglass" appearance. Endomyocardial biopsy revealed cardiac muscle cell disarray. We diagnosed a rare pediatric case of hypertrophic cardiomyopathy with mid-ventricular obstruction. This case reconfirms that electrocardiography during school health examinations is a very important screening tool for the detection of asymptomatic or mild symptomatic cardiac diseases.

Valvular heart disease

Diagnosis Aortic stenosis Patients with aortic stenosis can have chest X-ray findings showing dilation of the ascending aorta, but they may also have a completely normal chest X-ray. Direct visualization of calcifications on chest X-ray is uncommon. Other findings include dilation of the left ventricle. ECG typically shows left ventricular hypertrophy in patients with severe stenosis, but it may also show signs of left heart strain. Echocardiography is the diagnostic gold standard, which shows left ventricular hypertrophy, leaflet calcification, and abnormal leaflet closure.

Heart murmur

Abrupt standing Squatting, by increasing afterload and increasing preload. Handgrip maneuver, by increasing afterload Valsalva maneuver. One study found the Valsalva maneuver to have a sensitivity of 65%, specificity of 96% in detecting hypertrophic obstructive cardiomyopathy (HOCM). Both standing and Valsalva maneuver will decrease venous return and subsequently decrease left ventricular filling, resulting in an increase in the loudness of the murmur of hypertrophic cardiomyopathy, since outflow obstruction is increased by decreasing preload. Alternatively, squatting increases systemic vascular resistance, increasing afterload and helping to hold the obstruction in a more open configuration, decreasing the murmur. Maximum handgrip exercise also results in a decrease in the loudness of the murmur. Post ectopic potentiation

Aortic Valvular Atresia -- Evaluation

The initial electrocardiogram classically shows right axis deviation, right ventricular hypertrophy, and right atrial enlargement, though it can also show a pattern considered normal for patient age. This is generally attributed to the hypoplastic left side of the heart, but there are a few reported cases of left axis deviation and rarely, left ventricular hypertrophy. There are occasionally problems with bundle branch conduction, and Wolff-Parkinson-White pattern, as well as right bundle branch block, have been reported. There is a reported lack of a Q wave in lead V6, and this has been reported as a possible exclusion marker for aortic valvular atresia. It should be noted, though, that the lack of this finding is not specific for aortic valvular atresia, as other congenital heart conditions or even normal infants may lack the Q wave in this lead. T wave depressions in leads I and II, as well as ST-segment depressions in the left precordial leads, have also frequently been reported. [5] [8]

List of MeSH codes (C14)

– heart failure, congestive – cardiomyopathy, dilated – dyspnea, paroxysmal – edema, cardiac – heart neoplasms – heart rupture – heart rupture, post-infarction – ventricular septal rupture – heart valve diseases – aortic valve insufficiency – aortic valve stenosis – aortic stenosis, supravalvular – williams syndrome – aortic stenosis, subvalvular – cardiomyopathy, hypertrophic – discrete subaortic stenosis – heart murmurs – heart valve prolapse – aortic valve prolapse – mitral valve prolapse – tricuspid valve prolapse – mitral valve insufficiency – mitral valve stenosis – pulmonary atresia – pulmonary valve insufficiency – pulmonary valve stenosis – leopard syndrome – pulmonary subvalvular stenosis – tricuspid atresia – tricuspid valve insufficiency – tricuspid valve stenosis

Apical hypertrophic cardiomyopathy (apical hypertrophy): an overview.

Clinical and laboratory data of apical hypertrophy were reviewed based on our experience of over 200 consecutive patients, of whom 126 patients were followed up by myself for more than 1 year (1 to 29 years). Emphasis was placed on various aspects of electrocardiography including the natural course and "wax and wane" phenomenon of giant negative T waves (GNT). Recent diagnostic modality, i.e., cardiac magnetic resonance imaging was also stressed. Apical hypertrophic cardiomyopathy (apical hypertrophy) was mainly discovered by annual health check including electrocardiography and characterized by giant negative T waves (GNT; -1.0-(-)4.2 mV) in the left precordial leads (V4 or V5) in middle-aged men. Transition from normal T wave to negative T wave required several years and remained usually unchanged thereafter. This change may occur rather abruptly on rare occasions. Disappearance of GNT may also occur slowly and progressively in patients, in whom apical aneurysm had developed. The diagnosis may be obtained with echocardiography, left ventriculography or ultrafast computed tomography, but was most accurate with cardiac magnetic resonance imaging, by which identification of the diversity of hypertrophy was achieved, because the multiple short-axis views were accurately obtained in addition to the exact long-axis view. Hypertrophy was not simple but quite complex in both morphology and grade. Gene abnormality may be present even in cases of apical hypertrophy. The prognosis of apical hypertrophy in Japan has been benign, and heart failure due to atrial fibrillation and left ventricular aneurysm due to the destruction of hypertrophied muscle are thought to have prognostic importance, but these were rare in our series.

A natural history of apical hypertrophic cardiomyopathy with development of an apical aneurysm formation: A case report following a quarter century.

We report the definite long-term natural history of a man with apical hypertrophic cardiomyopathy (ApHCM), who developed an apical aneurysm by the age of 60 years. At 33 years, his electrocardiogram (ECG) was nearly normal. T-wave inversions were first identified in leads V5-6 of an ECG at 36 years of age. Echocardiography first demonstrated a left ventricular (LV) lateral wall hypertrophy at 37 years of age. At 42 years, echocardiography showed the pattern of diastolic spade-like appearance of the LV cavity, confirming the ApHCM diagnosis. At 54 years, a late-peaking apical systolic gradient of 10 mmHg (velocity: 1.6 m/s) emerged. At 60 years, he had developed an apical aneurysm. Cardiac computed tomography revealed no significant major coronary artery stenosis. Thus, in our case, LV hypertrophy and apical high pressure in ApHCM advanced the formation of an apical aneurysm in the absence of coronary artery disease. <<bLearning objective:</b High apical systolic flow velocity of ≥1.5 m/s in apical hypertrophic cardiomyopathy (ApHCM) using echocardiography may be predictive of the development of apical aneurysm, and make us consider medical intervention by beta-blockers or verapamil to delay or prevent aneurysm formation. Because recent studies have demonstrated that ApHCM may be less benign than previously suspected, observation without medical attention for ApHCM might be hazardous.>.

Handgrip maneuver

Murmurs that are due to forward flowing of blood such as aortic stenosis, and hypertrophic cardiomyopathy decrease in intensity. The effect of reducing the intensity in forward flowing murmurs is much more evident in aortic stenosis rather than mitral stenosis. The reason for this is that there is a larger pressure gradient across the aortic valve. A complementary maneuver for differentiating disorders is the Valsalva maneuver, which decreases preload. See also Valsalva maneuver Preload Afterload References Cardiac procedures

Aortic Regurgitation -- History and Physical -- Physical Examination

AR is associated with widened pulse pressure as a result of systolic hypertension and decreased diastolic pressure. The apical LV impulse is hyperdynamic and displaced laterally and inferiorly. A prominent systolic thrill may be palpable at the base of the heart or suprasternal notch and over the carotid arteries. It is caused by the large forward stroke volumes and low aortic diastolic pressure. S1 is normal, but S2 is increased (with a dilated aortic root) or decreased (when the aortic leaflets are thickened). A high frequency, blowing, decrescendo, diastolic murmur is heard best third intercostal space along the left sternal border. It is easier to appreciate the murmur of AR at the end of expiration while the patient is leaning forward.  The murmur increases with squatting or isometric exercise and decreases with maneuvers that decrease blood pressure. This murmur is early diastolic with mild AR and becomes holodiastolic with severe AR.

Idiopathic hypertrophic subaortic stenosis.

The clinical and laboratory findings in 29 patients with idiopathic hypertrophic subaortic stenosis are presented. Dyspnoea during exercise, angina pectoris, syncope combined with left ventricular hyperthrophy on ECG and chest X-ray and a systolic ejection murmur at the apex and the left sternal border are the most important findings. The findings were different in patients below and above 30 years of age. Most of the patients below 30 were in function group I, had a normal heart volume on chest X-+ray, and syncope was related to exercise. All patients above 30 had symptoms, nearly all were in function groups II-IV and often complained of palpitations, had increased heart volume on chest X-ray, sign of enlarged left atrium or atrial fibrillation of ECG. Syncope was not related to exercise, but always associated with palpitation in patients above 35 years of age. Pathologic Q waves were found more often in the younger age group. The differential diagnosis is discussed in relation to fixed aortic stenosis, mitral valve disease, ventricular septal defect, coronary artery disease, and hypertrophic cardiomyopathy without outflow tract obstruction.

[Clinical significance of electrocardiographic P-terminal force in V1 in patients with hypertrophic cardiomyopathy].

The clinical usefulness of P-terminal force in lead V1 (P-TF) was evaluated in 49 patients with hypertrophic cardiomyopathy. These 49 patients were categorized as 17 with an abnormal P-wave (P-TF greater than or equal to 3.0 msec.mV: group A) and 32 with a normal P-wave (P-TF less than 3.0 msec.mV: group B). Systolic blood pressure response (delta SBP) during the treadmill exercise test was significantly less in the group A than in the group B (delta SBP: 36 +/- 22 mmHg, 58 +/- 26 mmHg, respectively). Left atrial dimension measured from the M-mode echocardiogram was 37.8 +/- 5.0 mm in the group A and 31.0 +/- 5.2 mm in the group B. These differences were statistically significant (p less than 0.05). Left ventricular end-diastolic pressure averaged 19.5 +/- 7.9 mmHg in the group A and 13.5 +/- 4.0 mmHg in the group B (p less than 0.05). When comparing the group A and B, negative dp/dt / positive dp/dt of the group A was significantly less (0.69 +/- 0.14, 0.90 +/- 0.18, respectively) and the time constant T of the group A was significantly prolonged (86 +/- 30 msec, 56 +/- 10 msec, respectively). According to classifications of hypertrophic cardiomyopathy, all patients with the obstructive type had an abnormal P-wave. On the contrary, the majority of patients with apical hypertrophy had a normal P-wave.(ABSTRACT TRUNCATED AT 250 WORDS)