“Tomorrow, is the first blank page of a 365 page book. Write a good one.” HAPPY NEW YEAR 2014 TO ALL CARDIOLOVERS!

When Actual daily Practice-Based Medicine contradicts to Evidence-Based Medicine -" A 50 Years old man with Hyperkalemia , monomorphic VT ,baseline tachycardic rhythm,then Asystole,Bradycardia , CKD and Failing to Treat TdP"

Hot to Quickly to estimate Blood Pressure By Pulse ( Pulse Site=Specific BP Range) ?

ICCU duty interesting cases ! ( Acute Pul.Embolsim )

A 30 years old man brought to ICCU by complain of new onset severe dyspnea without PND, Orthopnea , chest pain ....etc
W/o any history of DVD and leg swelling and long time bed rest which he was physically active BP 90/60 , HR 150 , RR-28 , no any other considerable addiction and family history of CAD and Blood test not shown hypercoagulable state, CXR had not considerable changes still , D dimer was not match to disease , after ECG shown typical view of PE and echo shown RV and RA dilatation, RV dysfunction , severe pul.hypertension , and pulmonary artery thormbosis recorded and CT angiography . but extremity doppler was not documented any clod and occlusion . After tPa infusion over 2 hours he compeletly calm and HR decreased and dyspnea slowly resolved .
Typical ECG of PE :
the most specific finding on an ECG is the classic S1Q3T3 pattern , but the most common finding non-specific ST-segment and T-wave chages.
Other coomonly reported findings include sinus tachycardia , Right bundle branch block .
Like chest radiography , the major utility of ECG is the diagnosis of PE is to rule out the other major diagnosis such as acute MI .

( Easy way to Reduce 14-18 million deaths in 10 years )

Cardiogenic Shock due to Acute MI with Preserved Ejection Fraction !

In these days humming of Heart failure with preserved EF peaked in the skies, but once we know from our primitive studies from medical school which Cardiogenic shock is the advanced form of severely LV/RV dysfunction ,  but there are some causes which having  the EF preserved of LV disorder . 

from our primitive studies we know which the following causes are those causes of CS which may have preserved the EF , Although , In inferior and Posterior wall MI , not only one ventricle involves , here we have both ventricular disorder which prompt PCI and IABP rescued the patient : 

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ECG as an Exact Available , cheap , and bedside tool similar to angiography for culprit artery detection on duty nights ! ( A Case of Inferior wall MI )

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The best new drug for Rate controlling without any harm for IHD and HF patients with different mechanism !

Lower Extremity Arterial Occlusion as a result of LVT in an asymptomatic Young Man ( Amazing Case ) !

Comparison of Anterior and Inferior Wall Myocardial Infarction

بازتاب گزارش کورس تعلمیات متداوم طبی کاردیولوژی در ژورنال طبی تخصصی کشور Cardiology CME course's reflection in the Journal of Afghanistan Postgraduate Medical Education Journal

“She blew more smoke toward me, a lazy game of cancer catch.”

Cigarette smoking (CS) continues to be a major health hazard, and it contributes significantly to cardiovascular morbidity and mortality.
Cigarette smoking impacts all phases of atherosclerosis from endothelial dysfunction to acute clinical events, the latter being largely thrombotic. Both active and passive (environmental) cigarette smoke exposure predispose to cardiovascular events. Whether there is a distinct direct dose-dependent correlation between cigarette smoke exposure and risk is debatable, as some recent experimental clinical studies have shown a non-linear relation to cigarette smoke exposure. The exact toxic components of cigarette smoke and the mechanisms involved in CS-related cardiovascular dysfunction are largely unknown, but CS increases inflammation, thrombosis, and oxidation of low-density lipoprotein cholesterol. Recent experimental and clinical data support the hypothesis that cigarette smoke exposure increases oxidative stress as a potential mechanism for initiating
cardiovascular dysfunction.

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Anatomic and Functional Features of Mitral Stenosis !

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ACCF-AHA guideline for management of Unstable Angina and Non-STEMI

How to Survive a heart attack when alone !?

Post-infarction Pericardial Tamponade !

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Complications of Myocardial Infarction !

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Third Overall Assembly of ACS ( Afghanistan Cardiology Society ) همآیش سرتاسری سوم انجمن قلبی وعایی (کاردیولوژی) افغانستان

Afghanistan Cardiology Society , Celebrated its third annual overall Assembly and dedicated Specialty certificates to 30 specialist who succeed to pass one month annual Cardiological CME/CPD course . 

Understanding Carotid Sinus Massage (Made Easy ) !

Differential Diagnosis of ST-Segment Deviation ( ST-Elevation and ST-Depression ) Made Easy !

Summary of Sinoatrial Exit Blocks and its types (Made Easy) !

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Non-atherosclerotic Causes of Ischemic Heart Disease ( MI Type , 2,3,4)

Sinoatrial Block ( Second Degree Type I Block ) EKG Cards -Made Easy

Use of the Electrocardiogram in Acute Myocardial Infarction for Coronary Mapping

In 80% of cases, the culprit vessel in inferior myocardial infarction (MI) is the right coronary artery. The circumflex artery is the culprit vessel in all other cases, with the rare exception of a distally extending inferoapical “wraparound” left anterior descending artery, which is suggested when there is concomitant STsegment elevation in the precordial leads.
This Picture is worth thousand of words . 

An Introduction to Parasternal short axis view(PSAX View) in Echocardiogram

EKG Card # 11 ( ECG made easy ) Electrical Conduction System of the Heart(Depolarization and

EKG card # 10th! Velocity of Conduction of Electrical Impulses (EKG made easy !)

New York Heart Association (Grading for dyspnoea, palpitation, fatigue and angina in patients with cardiovascular disease)

The New York Heart Association (NYHA) Functional Classification in a Patient with Heart Disease 
Overview: The New York Heart Association (NYHA) developed a functional classification for patients with heart disease. 
Patients: Heart disease must be present. 
Parameters: 
(1) limitations on physical activity 
(2) symptoms (undue fatigue palpitations dyspnea and/or anginal pain) with ordinary physical activity  
(3) status at rest
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ECG of the Month

1- What does this tracing shows ?

A) Right Ventricular Hypertrophy 

B) Acute Posterior Myocardial Infarction 

Correct answer:
a) Right ventricular hypertrophy
Discussion:
In this tracing, the QRS axis tends to the right axis deviation (RAD), which should make one think of right ventricular hypertrophy (RVH) first. After the RAD, all other diagnostic features of RVH are found in the precordial leads—namely tall R waves in the right precordial leads, a deep S wave in V6, and downsloping ST-T changes that are more prominent in the right precordial leads. This tracing has all of these features and is from a patient with primary pulmonary hypertension with RVH. In a tracing of acute posterior myocardial infarction, the ST segment is depressed more horizontally, and RAD and a deep S wave in V6 are not part of it.

Source: The Heart.org 

Happy hearts: Positivity plus exercise linked to lower CVD mortality

The association between a positive emotional state of mind and lower mortality in patients with ischemic heart disease is mediated by exercise, according to the results of a new study .

Patients with higher levels of positive affect, which reflects a pleasurable response to the environment and typically includes feelings of happiness, joy, excitement, contentment and enthusiasm, had a 42% lower risk of all-cause mortality at five years and were 50% more likely to participate in an exercise program than those with lower levels of positive affect.

In an adjusted regression model, there was no significant association between positive affect, as measured using the global mood scale (GMS), and cardiac-related hospitalizations. Ischemic heart disease patients with higher levels of positive affect on the GMS had a significant 42% lower risk of all-cause mortality at five years. In addition, these happier patients were also 48% more likely to exercise.

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Multi-systemic effects of ACE inhibitors

RAAS and ACEIs

Discovery of RAAS occurred more than a century ago when in 1898, Tigerstedt1 and Bergmann demonstrated the existence of a substance (subsequently named renin) in crude extracts of rabbit renal cortex that caused a sustained increase in arterial pressure. Further understanding of RAAS pathway was brought forth by discovery of ANG-I  and II by Skeggs  and colleagues in 1950s. Finally, corticalhormone Aldosterone was discovered whose release was mediated via Ang-II and there by establishing the role of RAAS system in the regulation of blood pressure, fluid and electrolyte balance in the body.fig 1 

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Localization of MI

Anatomoelectrocardiographic Localization of MI

Infarction Location/Coronary Vessel Involvement

An introduction to Parasternal Long axis view (PLAX) in Echocardiogram

Roles of Precordial thump and its SHOULD and SHOULDN'Ts in CPR

Although,  precordial thump is relatively ineffective for ventricular fibrillation, and it is no longer recommended for this rhythm. A precordial thump should be considered if cardiac arrest is confirmed rapidly following a witnessed and monitored (ECG) sudden collapse (VF or VT) if the defibrillator is not immediately at hand.

There is insufficient evidence to recommend for or against the use of the precordial thump for

witnessed onset of asystole caused by AV-conduction disturbance.

The precordial thump should not be used for unwitnessed cardiac arrest.

A precordial thump should not be used in patients with a recent sternotomy (eg. for coronary artery grafts or valve replacement), or recent chest trauma.

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Inferior Wall MI , right ventricular MI and right ventricular dysfunction interdependence !

Ventricular Free wall rupture after MI

Fat embolism clinical features , diagnosis ,management

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EKG appearance of Digitalis effect (made easy )

EKG Card # 9 - Action Potential ( depolarization and Repolarization ) made easy

EKG Card #8 -EKG machine ( Made easy )

EKG Card # 7 -Conduction system Components of the heart (Made Easy )

Reduced risk of dementia by Statin use ( Statins halved dementia risk in AF patients)

 Two new studies from Taiwan may have somewhat allayed concerns about cognitive dysfunction being a possible side effect of statins.These new data suggest that high-potency statins may reduce the incidence of dementia in patients with atrial fibrillation and in elderly patients. Nevertheless, before we can know for sure that statins may prevent dementia, a clinical trial confirming these findings is mandatory. Results showed an inverse relationship between statin use and dementia, with the risk of dementia reducing with increasing statin dose. This trend remained in different age, gender, and cardiovascular risk subgroups.The adjusted risks for dementia were significantly inversely associated with increased total or daily equivalent statin dosage. Patients who received the highest doses of statins had a threefold decrease in the risk of developing dementia. High-potency statins such as atorvastatin and rosuvastatin [Crestor, AstraZeneca] showed a significant inverse association with developing dementia in a dose-response manner. Higher doses of high-potency statins gave the strongest protective effects against dementia.All the statins except lovastatin were associated with a decreased risk for new-onset dementia when taken at higher daily doses. Lin suggested lovastatin may have shown different results as it has less cholesterol-lowering effect than other statins.Statins halved dementia risk in AF patientsuring a six-year follow-up, 2.1% of the patients taking statins developed dementia compared with 3.5% of the nonstatin group, a statistically significant difference (p=0.002).Other factors that were associated with a reduced risk of dementia included male sex and lower CHADS₂ score. History of MI, peripheral artery disease, coronary artery disease, chronic kidney disease, and valvular heart disease were not associated with new-onset dementia
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Systolic BP changes associated with 1-g increases in sodium intake

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