Pathophysiology of intermittent claudication

What is CVP ? Abnormalites of CVP , High Vs. Low and Unilateral Vs. Bilateral Concepts of CVP !

Which one do you prefer ? Medical Therapy or Myocardial Revascularization ? As a choice treatment of chronic coronary syndrome and stable angina

From ICCU to ICU bedside Echocardiography !

However, Bedside transthoracic echocardiography (TTE) provides rapid and noninvasive hemodynamic assessment of critically ill patients but is limited by the immediate availability of experienced sonographer .Noncardiologists   are  able to estimate LV function with reasonable accuracy using a hand-held unit in the ICU ,but,  indeed, noncardiologists  often fail to identify important cardiac abnormalities such as valvular disease and regional wall abnormalities, important cardiac causes of hemodynamic compromise such as cor pulmonale, acute valvular abnormalities, and intracardiac shunts as well as very complicated cases rather than LV function determination only  .
Its training should be mandatory  for all intensivists and anesthesiologist  because it is of particular importance .

For example,respiratory variation in inferior vena cava diameter may help predict the likelihood of fluid responsiveness, and measurement of flow across the aortic valve can be used to estimate cardiac output and calculate systemic vascular resistance.
 Inotropic therapy might be withheld from patients with hemodynamic impairment resulting from decreased LV function if the TTE was misinterpreted as normal. Conversely, a patient with normal LV function whose hypotension was due to hypovolemia or vasodilation might be inappropriately treated with an inotrope if LV function was incorrectly deemed to be abnormal. in a daily basis , the most common error was failure to recognize a decrease in LV function rather than misinterpreting normal LV function as abnormal.  

Common variations in papillary muscle anatomy in HCM

Choice of Drugs for Cardiac Arrhythmias

Symptomatic tachycardias and premature beats may be treated with a variety of antiarrhythmic drugs. These may be given intravenously in an emergency situation or orally for long-term treatment. These drugs either suppress the abnormal firing of pacemaker tissue or depress the transmission of impulses in tissues that either conduct too rapidly or participate in reentry.

The relative simplicity of antiarrhythmic drug therapy must be balanced against two disadvantages. One is that the drugs must be taken daily and indefinitely. The other is the risk of side effects. While side effects are a risk of all medication, those associated with antiarrhythmic drugs can be very hard to manage. They include proarrhythmia, the more-frequent occurrence of preexisting arrhythmias or the appearance of new arrhythmias as bad as or worse than those being treated.

Prominent Papillary Muscle or Papillary Fibroelastoma, Apically displaced papillary muscles,Solitary Papillary Muscle Hypertrophy

A 55 years old female , brought to the Echo Lab for perioperative assessment of non-cardiac surgery of the heart . She was known patient of hypertension , DM type 2 with normal physical examination . During echocardiography we found a mass in LV cavity ECG was normal with no axis deviation , and hypertrophy pattern . There was Cardiologist to cardiologist difference of opension about below answers of diagnosis of the following echocardiogram :

1- Prominent Papillary muscle .

2- Papillary Fibroblastoma 

3- Apically displaced anterolateral papillary muscle .

4-  Solitary Papillary Muscle Hypertrophy.

The apically displaced anterolateral papillary muscle was definedwhen the base of the papillary muscle was located at the apical one-third of the left ventricle.

An abnormal insertion of the papillary muscle was noted in some patients with ADPM. Some patients had papillary muscle inserted into the base of a mitral leaflet or directly into the LVOT.

Apical hypertrophic cardiomyopathy (ApHCM) is a subtype ofmhypertrophic cardiomyopathy (HCM), which is more frequently mfound in Asians than in Caucasians.Although it has been demonstrated that ApHCM is generally benign, cardiovascular complications are not uncommon and therefore, correct diagnosis of mthis entity is important. Twelve-lead electrocardiograms (ECGs) of ApHCM are characterized by a giant negative T (GNT) wave in precordial leads. Moreover, the depth of the GNT wave has been reported to be associated with the severity of apical thickening or with the ratio of apical-to-basal myocardial thickness. Therefore, in the presence of a GNT wave, a diagnosis of ApHCM has often been made in patients with apical hypertrophy, especially when the GNT wave cannot be explained otherwiseThe phenomenon of solitary papillary muscle hypertrophy is rare with only 2 references in the literature. Furthermore, giant negative T and U waves are 2 common electrocardiographic phenomena in hypertrophic cardiomyopathy and have been attributed to hypertrophy of the posterior papillary muscle. Solitary hypertrophy of the anterior papillary muscle might be a new echo-electrocardiographic syndrome.

Electrocardiogram and its images of apical hypertrophy. (A) T wave negativity more prominent in the mid-precordial than in the lateral precordial leads represent classic electrocardiographic finding in apical hypertrophy. (B) Representative echocardiography images of the classic pattern of apical hypertrophic cardiomyopathy showing an ‘ace of spade’ shape during diastole. (C) However, it is not unusual to encounter an atypical pattern of hypertrophy showing more prominent hypertrophy at the apical lateral than at the apical septal segments.

Various patterns of anterolateral papillary muscle location in the apical four-chamber view. (A) Normally located papillary muscle . (B) Apically displaced papillary muscle . (C) Variation in the morphology of papillary muscle head attached to the left ventricular (LV) . (D) Apically attached accessory papillary muscle. (E) The papillary muscle inserted into the base of a mitral valve leaflet . (F) The papillary muscle inserted into the left ventricular outflow tract . An apicoseptal segment may also show certain degree of hypertrophy, but for the clarity of presentation, this finding is not represented in above fig.

Anothoer distinc feature of papillary muscle is Papillary fibroelastoma, or papilloma, is a benign intracardiac tumor with a characteristic appearance on echocardiograms. It is usually small (average size, <15 mm) and has a characteristic stippled edge, with a shimmering appearance at the tumor-blood interface. There are f ingerlike projections consistent with the fronds that are described pathologically as a “sea anemone.” The most frequent location is the aortic valve on either the aortic or ventricular surface, followed by either the atrial or ventricular surface of the mitral valve.138 Papillomas can be found in any chamber or on any surface and are usually single, but multiple tumors occur in approximately 10% of patients.

Solitary Papillary Muscle Hypertrophy: Transthoracic, two-dimensional echocardiography revealed isolated hypertrophy of the anterolateral papillary muscle, with an otherwise normal left ventricle with no hypertrophy in any other segment( image below) .  

The answer is A. Prominent Papillary Muscle . 

Dilated Cardiomyopathy and Myocardial Infarction

•  Cardiac magnetic resonance (CMR) is the current golden standard for accurate assessment of ventricular volumes and global and regional function, thus providing information on prognosis.

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    Extracellular accumulation of gadolinium, imaged at 10 to 30 minutes after injection, identifies areas of myocardial fibrosis commonly seen in cardiomyopathies, generally subendocardial or transmural in a coronary distribution in the case of ischemic cardiomyopathy.

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    Transmural extent of LGE can predict recovery of myocardial function after revascularization in patients with coronary artery disease.

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    Negative stress CMR with either adenosine or dobutamine stressors has excellent negative predictive value for subsequent coronary events.

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    Noncoronary segmental distribution and midwall or epicardial involvement of LGE are atypical of myocardial infarction. This allows discrimination between ischemic and nonischemic etiologies of cardiomyopathy, which can assist in clinical decision making.

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    Takotsubo cardiomyopathy is characterized by left ventricular apical dilation and regional hypocontraction, absence of first-pass perfusion abnormality, and minimal or absent concomitant subendocardial LGE.

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    Because of its higher spatial and temporal resolution, CMR can offer an improved assessment for the presence and extend of ventricular noncompaction, compared with echocardiography.

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    CMR can accurately quantify severity of valvular regurgitation and stenosis using phase contrast imaging. In the same study CMR can assess the physiologic impact of the valvular heart disease by providing quantitation of large vessel morphology and ventricular volumes and functions.

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    CMR is the most sensitive technique for detecting clinically unrecognized small subendocardial myocardial infarctions that do not result in wall motion abnormality or ECG changes, thereby identifying patients at risk of cardiac events.

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    CMR infarct imaging can provide direct information on the amount of irreversibly injured myocardium and viable myocardium, including the extent of periinfarct zone and microvascular obstruction, which are strong predictors of cardiovascular outcome in patients after myocardial infarction (MI).

   Case: A 54-year-old woman without significant risk factors for coronary artery disease presented to our services complaining of a 4-week history of exertional dyspnea (NYHA class III) and pedal edema. The patient did not have any history of alcoholism, family history of heart disease, or sudden cardiac death. ECG showed sinus rhythm and a left bundle branch block pattern of unknown duration. Transthoracic echocardiography showed a dilated left ventricle and severe global hypokinesis with reduced ejection fraction of 25%. A coronary angiography was performed that revealed no significant coronary stenosis. CMR was performed .
  
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